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Novel Role of Pin1-Cis P-Tau-ApoE Axis in the Pathogenesis of Preeclampsia and Its Connection with Dementia
Beyond Amyloid and Tau: The Critical Role of Microglia in Alzheimer’s Disease Therapeutics
Postbiotics Improve Colorectal Cancer–Macrophage Cross-Talk
Anti-Drug Antibody Responses and Mitigation Strategies
Urobilin May Interfere with Bilirubin Interacting with Albumin: Implications for Disease Pathology

Journal Description

Biomedicines

Biomedicines is an international, peer-reviewed, open access journal on biomedicines published monthly online by MDPI.

Open Access— free for readers, with article processing charges (APC) paid by authors or their institutions.
High Visibility: indexed within Scopus, SCIE (Web of Science), PubMed, PMC, CAPlus / SciFinder, and other databases.
Journal Rank: JCR - Q1 (Pharmacology and Pharmacy) / CiteScore - Q2 (Medicine (miscellaneous))
Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 14.6 days after submission; acceptance to publication is undertaken in 2.8 days (median values for papers published in this journal in the second half of 2024).
Recognition of Reviewers: reviewers who provide timely, thorough peer-review reports receive vouchers entitling them to a discount on the APC of their next publication in any MDPI journal, in appreciation of the work done.
Companion journals for Biomedicines include: IJTM, BioMed, Anesthesia Research and Emergency Care and Medicine.

Impact Factor: 3.9 (2023); 5-Year Impact Factor: 4.1 (2023)

Imprint Information Journal Flyer Open Access ISSN: 2227-9059

Latest Articles

14 pages, 1330 KiB

Open AccessArticle

Assessment of Levels of Apelinergic System Peptides in Serum and Epicardial Adipose Tissue in Patients with Multivessel Coronary Artery Disease Who Underwent Myocardial Revascularisation

by Maciej Rachwalik, Anna Leśków, Małgorzata Matusiewicz, Agnieszka Jama-Kmiecik and Dorota Diakowska

Biomedicines 2025, 13(4), 809; https://doi.org/10.3390/biomedicines13040809 (registering DOI) - 27 Mar 2025

Background: Peptides of the apelinergic system may participate in the development of atherosclerosis, but their role in atherogenesis is unclear. The aim of the study was to evaluate the levels of apelinergic system peptides, such as Elabela (Ela), apelin-13 (AP-13), apelin-17 (AP-17) and [...] Read more.

Background: Peptides of the apelinergic system may participate in the development of atherosclerosis, but their role in atherogenesis is unclear. The aim of the study was to evaluate the levels of apelinergic system peptides, such as Elabela (Ela), apelin-13 (AP-13), apelin-17 (AP-17) and apelin receptor (APJ) in the serum and epicardial adipose tissue (EAT) of patients with multivessel coronary artery disease (CAD) who underwent myocardial revascularisation surgery. Methods: The participants comprised 51 CAD patients and 34 healthy adults. Concentrations of Ela, AP-13, AP-17 and APJ were determined by ELISA kits. We analysed the demographics, and clinical and laboratory parameters of the CAD patients. Results: We showed that the serum Ela and AP-17 levels significantly decreased, and APJ significantly increased, in the CAD patients in comparison to the healthy control. A significant relationship between the serum and EAT concentrations of Ela and APJ (p < 0.05) was observed. Positive correlations were found between the serum levels of AP-13 and AP-17, and between AP-17 and APJ. There was a positive correlation between the tissue levels of AP-17 and APJ. The tissue Ela concentration negatively correlated with the BMI, TCH and LDL levels. AP-13 in EAT was negatively associated with the glucose level. In contrast, the tissue APJ showed a positive correlation with TCH concentration. Good diagnostic potential of ELA, AP-17 and APJ was observed for CAD prediction (p < 0.001 for all). Conclusions: The results indicate that the levels of apelinergic peptides are altered in patients with CAD, which may be a potential diagnostic indicator. Full article

(This article belongs to the Special Issue Recent Advances in Adipokines—2nd Edition)

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8 pages, 389 KiB

Open AccessOpinion

Pulmonary Hypertension-Related Interstitial Lung Disease: An Expert Opinion with a Real-World Approach

by Rachel N. Criner, Mario Naranjo, Gilbert D’Alonzo and Sheila Weaver

Biomedicines 2025, 13(4), 808; https://doi.org/10.3390/biomedicines13040808 (registering DOI) - 27 Mar 2025

Great progress has been made in the treatment of pulmonary arterial hypertension (WHO group 1 PAH) over the past two decades, which has significantly improved the morbidity and mortality in this patient population. Likewise, the more recent availability of antifibrotic medications for interstitial [...] Read more.

Great progress has been made in the treatment of pulmonary arterial hypertension (WHO group 1 PAH) over the past two decades, which has significantly improved the morbidity and mortality in this patient population. Likewise, the more recent availability of antifibrotic medications for interstitial lung disease (ILD) have also been effective in slowing down the progression of disease. There is no known cure for either of these disease states. When this combination coexists, treatment can be challenging. Interstitial lung disease is a heterogenous group of chronic inflammatory and/or fibrotic parenchymal lung disorders. A subset of patients with ILD, not related to connective tissue disease, can initially present with inflammatory-predominant disease which progresses to irreversible fibrosis. This population of patients is also at risk for developing pulmonary hypertension (PH) or World Health Organization (WHO) group 3 PH. This coexistence of ILD and PH is associated with early morbidity and mortality. The early identification, diagnosis, and treatment of this combination of ILD and PH is vital. Medications available for both ILD and PH require an individualized approach with the intention of slowing down disease progression. Referral to expert centers for clinical trials and transplant evaluation is recommended. The combination of PH-ILD can be challenging to diagnose and treat effectively. Patients require a thorough clinical evaluation to enable the most accurate diagnosis. A vital part of that evaluation is the early recognition of PH. Medications can help improve disease progression along with clinical trials that will further improve our gaps in knowledge. Full article

(This article belongs to the Special Issue Feature Reviews in Cardiovascular Diseases)

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13 pages, 1828 KiB

Open AccessArticle

Low Vitamin K Status and Risk of Chronic Obstructive Pulmonary Disease

by Daniel Alexander Ackermann, Allan Linneberg, Ema Rastoder, Anna Kubel Vognsen, Anne Ahrendt Bjerregaard, Lennart Friis-Hansen, Niklas Rye Jørgensen, Caroline Emma Hedsund, Niklas Dyrby Johansen, Daniel Modin, Maria Dons, Mats C. Højbjerg Lassen, Kristoffer Grundtvig Skaarup, Ditte Vesterlev, Mia Moberg, Julie Janner, Josefin Eklöf, Lars Pedersen, Elisabeth Bendstrup, Christian B. Laursen, Jørn Carlsen, Tor Biering-Sørensen, Jens-Ulrik Stæhr Jensen and Pradeesh Sivapalan Show full author list Hide full author list

Biomedicines 2025, 13(4), 807; https://doi.org/10.3390/biomedicines13040807 (registering DOI) - 27 Mar 2025

Background: Vitamin K is a cofactor necessary for the biological activity of proteins like Matrix Gla Protein (MGP), which reduce calcification and help preserve lung function. This study aims to determine, first, whether low vitamin K status is associated with chronic obstructive pulmonary [...] Read more.

Background: Vitamin K is a cofactor necessary for the biological activity of proteins like Matrix Gla Protein (MGP), which reduce calcification and help preserve lung function. This study aims to determine, first, whether low vitamin K status is associated with chronic obstructive pulmonary disease (COPD), and secondary, whether the level of vitamin K is associated with COPD severity, smoking exposure, or mortality. Methods: The plasma concentration of dephosphorylated uncarboxylated (dp-uc) MGP was used as an inverse biomarker for vitamin K in 98 COPD patients from the CODEX-P COPD study and 986 controls from the DanFunD study. Low vitamin K status was defined as the upper quartile of dp-ucMGP (>589 pmol/L). Using a logistic regression model, we examined whether low vs. high/moderate vitamin K status increased the odds ratio (OR) of having COPD. Secondary analyses, in the COPD cohort only, examined the association between low vitamin K status and COPD severity, smoking exposure in packyears and all-cause mortality, using a Welch’s t-test and log-rank test, respectively. Results: Low vitamin K status was associated with increased odds of having COPD, OR 9.7 (95% CI [5.5 to 17.5], p < 0.001). We found no associations between low vitamin K and COPD severity (est. −0.03, p = 0.7; 95% CI [−0.2 to 0.1]), smoking exposure (p = 0.7), or all-cause mortality (p = 0.5). Conclusions: Low vitamin K status was associated with substantially higher odds of having COPD compared to high/moderate vitamin K status. No association was found between low vitamin K status and COPD severity, smoking exposure, or all-cause mortality. Further studies are needed to determine if vitamin K plays a role in the pathophysiology of COPD and whether supplement therapy is indicated. Full article

(This article belongs to the Section Molecular and Translational Medicine)

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11 pages, 3802 KiB

Open AccessArticle

A Combined Approach Using Strip Grafts and Xenogenic Dermal Matrix for Peri-Implant Keratinized Mucosa Augmentation in the Mandible: A Case Series

by Xinda Li, Dániel Palkovics, Péter Windisch, Željka Perić Kačarević and Attila Horváth

Biomedicines 2025, 13(4), 806; https://doi.org/10.3390/biomedicines13040806 (registering DOI) - 27 Mar 2025

Background: Ensuring a minimum peri-implant keratinized mucosa width (PIKM-W) is critical for maintaining dental implant health, as inadequate PIKM-W is associated with increased risks of plaque accumulation, mucosal inflammation, and peri-implantitis. While epithelialized connective tissue grafts (ECTGs) are considered the gold standard for [...] Read more.

Background: Ensuring a minimum peri-implant keratinized mucosa width (PIKM-W) is critical for maintaining dental implant health, as inadequate PIKM-W is associated with increased risks of plaque accumulation, mucosal inflammation, and peri-implantitis. While epithelialized connective tissue grafts (ECTGs) are considered the gold standard for soft tissue augmentation, they often lead to significant patient morbidity. Xenogeneic dermal matrices (XDMs) offer a less invasive alternative, but are prone to shrinkage, particularly in the mandible. The aim of this study was to evaluate a new surgical method to overcome these limitations with the combination of a narrow band of ECTG (autogenous strip graft, ASG) and an XDM to augment the PIKM-W in the posterior mandible. Methods: Twelve patients with a PIKM-W of less than 2 mm in the mandible underwent peri-implant soft tissue augmentation using this combined approach. Changes in the PIKM-W were measured preoperatively; immediately postoperatively; and at 1, 3, 6, 9, and 12 months. Graft remodeling (shrinkage or contraction) and PIKM thickness (PIKM-T) were also evaluated over time. Results: Preoperatively, the mean PIKM-W was 0.39 ± 0.40 mm and the PIKM-T was 1.36 ± 0.43 mm. At 6 months, the mean PIKM-W was 4.93 ± 0.98 mm and the PIKM-T was 2.88 ± 0.80 mm, with shrinkage of 39.2 ± 14.1%. By 12 months, the mean PIKM-W stabilized at 4.58 ± 1.28 mm and the PIKM-T stabilized at 2.83 ± 0.65 mm, with shrinkage of 42.2% ± 16.8%. Conclusions: There were statistically significant differences in clinical parameters between the baseline and 6 and 12 months (p < 0.05). This technique demonstrated the potential for stable augmentation of PIKM-W and PIKM-T over time, with manageable shrinkage. However, further studies with larger sample sizes are needed to confirm its clinical efficacy as an alternative for mandibular keratinized mucosa augmentation around implants. Full article

(This article belongs to the Section Molecular and Translational Medicine)

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27 pages, 1365 KiB

Open AccessReview

From Discovery to Innovative Translational Approaches in 80 Years of Fragile X Syndrome Research

by Mathijs B. van der Lei and R. Frank Kooy

Biomedicines 2025, 13(4), 805; https://doi.org/10.3390/biomedicines13040805 (registering DOI) - 27 Mar 2025

Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a major genetic contributor to autism spectrum disorder. It is caused by a CGG trinucleotide repeat expansion in the FMR1 gene, resulting in gene silencing and the loss of [...] Read more.

Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a major genetic contributor to autism spectrum disorder. It is caused by a CGG trinucleotide repeat expansion in the FMR1 gene, resulting in gene silencing and the loss of FMRP, an RNA-binding protein essential for synaptic plasticity. This review covers over 80 years of FXS research, highlighting key milestones, clinical features, genetic and molecular mechanisms, the FXS mouse model, disrupted molecular pathways, and current therapeutic strategies. Additionally, we discuss recent advances including AI-driven combination therapies, CRISPR-based gene editing, and antisense oligonucleotides (ASOs) therapies. Despite these scientific breakthroughs, translating preclinical findings into effective clinical treatments remains challenging. Clinical trials have faced several difficulties, including patient heterogeneity, inconsistent outcome measures, and variable therapeutic responses. Standardized preclinical testing protocols and refined clinical trial designs are required to overcome these challenges. The development of FXS-specific biomarkers could also improve the precision of treatment assessments. Ultimately, future therapies will need to combine pharmacological and behavioral interventions tailored to individual needs. While significant challenges remain, ongoing research continues to offer hope for transformative breakthroughs that could significantly improve the quality of life for individuals with FXS and their families. Full article

(This article belongs to the Special Issue Diagnostic Biomarkers and Novel Therapeutics Targets for Fragile X Syndrome, Autism Spectrum Disorders and Genetic Neurodevelopmental Diseases: Advances and Challenges)

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12 pages, 2152 KiB

Open AccessArticle

Fragmented QRS in Lateral Leads on Electrocardiography Is Associated with Cardiac Dysfunction and Left Ventricular Dilation in Duchenne Muscular Dystrophy

by Tetsushi Yamamoto, Shuichiro Ogawa, Yusuke Ide, Kokoro Miyazaki, Aiko Sunami, Yoshinori Nambu, Ryosuke Bo, Masafumi Matsuo and Hiroyuki Awano

Biomedicines 2025, 13(4), 804; https://doi.org/10.3390/biomedicines13040804 (registering DOI) - 27 Mar 2025

Background/Objectives: Duchenne muscular dystrophy (DMD) is an X-linked inherited muscle disease. Patients with DMD demonstrate improved prognosis with angiotensin-converting enzyme inhibitors and beta-blockers at the time of cardiac dysfunction. However, most deaths due to DMD are due to cardiac dysfunction. Fragmented QRS [...] Read more.

Background/Objectives: Duchenne muscular dystrophy (DMD) is an X-linked inherited muscle disease. Patients with DMD demonstrate improved prognosis with angiotensin-converting enzyme inhibitors and beta-blockers at the time of cardiac dysfunction. However, most deaths due to DMD are due to cardiac dysfunction. Fragmented QRS (fQRS) is an abnormal finding that forms a notch in the QRS wave on electrocardiography (ECG) and is associated with fibrosis and scarring of the myocardium. Methods: Patients with DMD were examined for the number of leads of fQRS, their sites of appearance, changes in cardiac dysfunction, and age using the chest leads of a synthesized 18-ECG. A retrospective analysis of 184 patients under 20 years of age with DMD and known genetic mutations was performed; they were divided into three age groups: 3–10, 11–15, and 16–20 years. The chest leads of the ECG were defined as follows: V1-3, anterior leads; V4-6, lateral leads; V7-9, posterior leads; and V3R-V5R, right-sided chest leads. Cardiac dysfunction was defined as a left ventricular (LV) ejection fraction <53% on the same day, and echocardiography was performed. LV dilation was defined as dilation beyond the normal range, considering the body surface area. Results: In 167 of 184 patients (91%), fQRS was present in one or more chest leads. The number of fQRS leads in the anterior and lateral walls was significantly higher in 16–20-year-olds than in 3–10-year-olds. The total number of chest leads with fQRS was 4.9 ± 3.1 in the cardiac dysfunction group and 3.5 ± 2.5 in the preserved group. The cardiac dysfunction group had a significantly greater number of fQRS leads than did the preserved group (p = 0.003). The group with LV dilation had a significantly greater number of fQRS leads than did the non-dilation group (p = 0.009). Conclusions: The fQRS site is associated with age, cardiac dysfunction, and LV dilation. Multivariate regression analysis revealed that the number of anterior leads of the fQRS correlated with age and that of lateral leads of the fQRS with cardiac dysfunction and LV dilation. The number of fQRS leads on the lateral wall marks cardiac dysfunction and LV dilation. Full article

(This article belongs to the Special Issue Diagnosis, Pathogenesis and Treatment of Muscular Dystrophy)

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18 pages, 1256 KiB

Open AccessArticle

The Effect of Naturally Acquired Immunity on Mortality Predictors: A Focus on Individuals with New Coronavirus

by Mónica Queipo, Jorge Mateo, Ana María Torres and Julia Barbado

Biomedicines 2025, 13(4), 803; https://doi.org/10.3390/biomedicines13040803 (registering DOI) - 27 Mar 2025

Background/Objectives: The spread of the COVID-19 pandemic has spurred the development of advanced healthcare tools to effectively manage patient outcomes. This study aims to identify key predictors of mortality in hospitalized patients with some level of natural immunity, but not yet vaccinated, [...] Read more.

Background/Objectives: The spread of the COVID-19 pandemic has spurred the development of advanced healthcare tools to effectively manage patient outcomes. This study aims to identify key predictors of mortality in hospitalized patients with some level of natural immunity, but not yet vaccinated, using machine learning techniques. Methods: A total of 363 patients with COVID-19 admitted to Río Hortega University Hospital in Spain between the second and fourth waves of the pandemic were included in this study. Key characteristics related to both the patient’s previous status and hospital stay were screened using the Random Forest (RF) machine learning technique. Results: Of the 19 variables identified as having the greatest influence on predicting mortality, the most powerful ones could be identified at the time of hospital admission. These included the assessment of severity in community-acquired pneumonia (CURB-65) scale, age, the Glasgow Coma Scale (GCS), and comorbidities, as well as laboratory results. Some variables associated with hospitalization and intensive care unit (ICU) admission (acute renal failure, shock, PRONO sessions and the Acute Physiology and Chronic Health Evaluation [APACHE-II] scale) showed a certain degree of significance. The Random Forest (RF) method showed high accuracy, with a precision of >95%. Conclusions: This study shows that natural immunity generates significant changes in the evolution of the disease. As has been shown, machine learning models are an effective tool to improve personalized patient care in different periods. Full article

(This article belongs to the Special Issue The End of the COVID-19 Pandemic—What Is Currently Known and What Could Have Been Useful Four Years Ago? (2nd Edition))

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17 pages, 11450 KiB

Open AccessArticle

Electroacupuncture Attenuates Intestinal Barrier Disruption via the α7nAChR-Mediated HO-1/p38 MAPK/NF-κB Pathway in a Mouse Model of Metabolic Dysfunction-Associated Fatty Liver Disease: A Randomized, Single-Blind, Controlled Trial

by Xiao Wang, Jiasen Sun, Peng Wang, Yimin Zhang, Jiuyang Chang and Zhijun Duan

Biomedicines 2025, 13(4), 802; https://doi.org/10.3390/biomedicines13040802 (registering DOI) - 27 Mar 2025

Background: Gut barrier integrity plays a crucial role in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD). Electroacupuncture (EA) at ST-36 can ameliorate inflammatory responses via stimulating the α7 nicotinic acetylcholine receptor (α7nAChR), but whether EA is effective in preserving the intestinal [...] Read more.

Background: Gut barrier integrity plays a crucial role in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD). Electroacupuncture (EA) at ST-36 can ameliorate inflammatory responses via stimulating the α7 nicotinic acetylcholine receptor (α7nAChR), but whether EA is effective in preserving the intestinal barrier of MAFLD has not been exactly illustrated. This investigation explored potential protection mechanisms of EA at ST-36 targeting the dismantled gut barrier in MAFLD. Methods: C57BL/6 mice were randomly allocated into several subgroups: control (CON), high-fat diet (HFD), HFD with EA, HFD with EA and α7nAChR inhibitor α-BGT, and HFD with EA and intestinal HO-1 knockout (KO). Body weight, liver weight, visceral fat index, and histopathological examination of the liver and the intestine were determined. Serum biological indexes were evaluated through corresponding kits. Furthermore, the expressions of HO-1, α7nAChR, gut barrier-associated proteins, and the molecular mechanisms in intestinal tissues were assessed via Western blot, RT-qPCR, immunohistology, or immunofluorescence examination. Results: EA treatment decreased body weight, liver weight, and visceral fat index gain and mitigated liver function injury and abnormal lipid indexes, exhibiting less severity of hepatic steatosis, fibrosis, and inflammation responses of MAFLD. Lower gut permeability, less intestinal epithelial disruption, and upregulation of tight junction proteins after EA suggested the protective effects in attenuating intestinal epithelial barrier dysfunction. These protective effects were abolished by α-BGT or intestinal HO-1 deletion. Mechanistically, EA markedly enriched α7nAChR and HO-1 expression and mitigated phosphorylated p38 MAPK/NF-κB activation, which was lost in α-BGT or HO-1 KO treatment. Conclusions: The protective effects of EA at ST-36 in the pathogenesis of MAFLD may be attributed to the preserved intestinal barrier, thereby alleviating systemic inflammatory responses and preventing subsequent liver hits, where the α7nAChR-mediated HO-1/p38 MAPK/NF-κB pathway was crucial to maintain homeostasis. Full article

(This article belongs to the Section Cell Biology and Pathology)

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22 pages, 2080 KiB

Open AccessReview

Desensitization for Vitamin B12 Hypersensitivity and How to Do It

by Kinga Lis

Biomedicines 2025, 13(4), 801; https://doi.org/10.3390/biomedicines13040801 (registering DOI) - 26 Mar 2025

Vitamin B12 is the common name for a group of cobalamins, which are cobalt corrines. Cobalamins are water-soluble B vitamins. Vitamin B12, as a coenzyme of various enzymes, is an essential component of many key metabolic processes in the body. Vitamin B12 deficiency [...] Read more.

Vitamin B12 is the common name for a group of cobalamins, which are cobalt corrines. Cobalamins are water-soluble B vitamins. Vitamin B12, as a coenzyme of various enzymes, is an essential component of many key metabolic processes in the body. Vitamin B12 deficiency causes dysfunction of various organs and systems in the body, including the central nervous system. Humans, like other animals, are unable to synthesize cobalamin. This vitamin must be supplied with a balanced diet. The only valuable dietary sources of cobalamin are foods of animal origin, especially offal (e.g., liver). Vegan and vegetarian diets are deficient in vitamin B12. People who follow this nutritional model require systematic cobalamin supplementation, usually in oral form. Other causes of cobalamin deficiency are various pathogenetic processes, in the course of which any of the stages of the complicated process of absorption of this vitamin from the gastrointestinal tract are impaired. Disorders of intestinal absorption of vitamin B12 require systematic supplementation of cobalamin parenterally (usually by intramuscular or subcutaneous injections) for the rest of life. Supplementary therapy with vitamin B12 may cause various adverse reactions, among which hypersensitivity reactions of various spectrums and intensity of symptoms are possible. According to available data, hypersensitivity to cobalamin is more likely after intramuscular or subcutaneous administration than in oral form. It also seems that long-term administration of cobalamin predisposes to allergy to vitamin B12, regardless of its chemical form. Although hypersensitivity to cobalamin is rather rare, it can also be of great clinical importance. This is due to the fact that vitamin B12 deficiency affects a significant part of the population, especially the elderly and those with chronic diseases that impair its absorption. In addition, supplementary therapy with cobalamin is long-term (usually lifelong) and there is no alternative form of treatment. For these reasons, solutions are sought that will allow for the safe continuation of treatment supplementing cobalamin deficiency. Various cyanocobalamin desensitization protocols are proposed, differing in duration, the dynamics of gradual dose increase, or the method of injection (intramuscular or subcutaneous). An analysis of available data in this field suggests that desensitization with cyanocobalamin seems to be an effective way to obtain tolerance to vitamin B12, allowing for long-term supplementation of this vitamin regardless of the chemical form, dose size, frequency, or route of administration. Full article

(This article belongs to the Special Issue Convergence of Allergology and Immunology: Unveiling Mechanistic Insights)

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14 pages, 1610 KiB

Open AccessArticle

Transpulmonary LOX-1 Levels Are Predictive of Acute Respiratory Distress Syndrome After Cardiac Surgery: A Proof-of-Concept Study

by Benjamin Deniau, Pierre-Olivier Ludes, Pamela Khalifeh-Ballan, Luc Fenninger, Michel Kindo, Olivier Collange, Bernard Geny, Eric Noll, Fériel Azibani, Alexandre Mebazaa and Julien Pottecher

Biomedicines 2025, 13(4), 800; https://doi.org/10.3390/biomedicines13040800 (registering DOI) - 26 Mar 2025

Background/Objectives: Acute respiratory distress syndrome (ARDS) is a life-threatening condition that frequently complicates high-risk cardiac surgery. We evaluated the circulating levels and transpulmonary gradient of intracellular proteins in patients at risk of developing ARDS after cardiac surgery using large scale-proteomics. Methods: We enrolled [...] Read more.

Background/Objectives: Acute respiratory distress syndrome (ARDS) is a life-threatening condition that frequently complicates high-risk cardiac surgery. We evaluated the circulating levels and transpulmonary gradient of intracellular proteins in patients at risk of developing ARDS after cardiac surgery using large scale-proteomics. Methods: We enrolled sixteen patients undergoing high-risk cardiac surgery, followed by planned ICU admission. Circulating levels of intracellular proteins were measured at the onset of the surgical procedure, at ICU admission (H0), and 24 h (H24) after surgery in blood samples simultaneously drawn from both the pulmonary artery and the left atrium. The primary endpoint was the occurrence of ARDS between ICU admission and the subsequent 48 h. Results: Among the studied proteins, the levels of intracellular lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) were higher at H24 in the pulmonary artery in patients who developed ARDS (6.96; 95% CI [6.83–7.23]) compared to patients who did not (6.48; 95% CI [6.27–6.66]), p-value = 0.016. The transpulmonary gradient of intracellular LOX-1 levels was not significantly different between ARDS and non-ARDS patients at H0 but it was more negative at H24 in ARDS (−0.23; 95% CI [−0.27, −0.14]) than in non-ARDS patients (0.03; 95% CI [−0.14, 0.32]; p-value= 0.031), with a hazard ratio HR = 0.39 (95% CI [0.18–0.86]); p-value= 0.035. The area under the ROC curve of H24 LOX-1 transpulmonary gradient to predict ARDS occurrence was 0.83 (95% CI [0.62–1.00]). Conclusions: The transpulmonary gradient of intracellular LOX-1 levels was negatively associated with the occurrence of ARDS within the first 48 h after high-risk cardiac surgery, suggesting that lung trapping of LOX-1 may be linked to postoperative ARDS. Full article

(This article belongs to the Special Issue Research Trends in Cardiovascular Pathologies: From Mechanisms to Therapies)

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22 pages, 7028 KiB

Open AccessArticle

Migrasome-Related Genes as Potential Prognosis and Immunotherapy Response Predictors for Colorectal Cancer

by Lu Chang, Chao Qin, Yimin Chu, Ming Guan and Xuan Deng

Biomedicines 2025, 13(4), 799; https://doi.org/10.3390/biomedicines13040799 (registering DOI) - 26 Mar 2025

Background: Studies highlight the role of migrasomes as mediators of intercellular communication and signaling, critical in influencing tumorigenesis and progression. Yet migrasome-related genes and their potential role in colorectal cancer prognosis remain unexplored. Methods: Differentially expressed gene set A (DEG set A) was [...] Read more.

Background: Studies highlight the role of migrasomes as mediators of intercellular communication and signaling, critical in influencing tumorigenesis and progression. Yet migrasome-related genes and their potential role in colorectal cancer prognosis remain unexplored. Methods: Differentially expressed gene set A (DEG set A) was identified in the TCGA-CRC dataset, and Weighted Gene Co-expression Network Analysis (WGCNA) was performed to identify the most important modules associated with migrasome-related gene (MRG) scores. Single-cell RNA-seq dataset GSE231559 DEG set B was determined. Candidate migrasome-related genes were filtered by intersecting DGE set A, key module genes, and DEG set B. Prognostic genes were subsequently screened through regression analysis, and a risk model was developed. Patients with CRC in the TCGA cohort were stratified into high- and low-risk groups based on the optimal cutoff of the risk score. Immunotherapy response-related analyses were then performed. Finally, cell-to-cell communication analysis was carried out for key cells identified based on prognostic gene expression analysis in annotated cells. Results: The six candidate migrasome-related genes were identified through the overlap of 5158 DEG set A, 1960 key module genes, and 146 DEG set B. Further screening led to the selection of T1MP1, CXCL8, and MGP as potential prognostic biomarkers. Immune-related analysis indicated that the high-risk group exhibited a better response to immunotherapy. Notably, the prognostic genes showed elevated expression levels in monocytes and tissue stem cells, thereby designating them as key cell types. Conclusions: We conducted bioinformatic analysis of migrasome-related genes and identified significant involvement of T1MP1, CXCL8, and MGP in influencing CRC prognosis and immunotherapy response. Our research provides novel insights into the role of migrasomes in CRC biology. Full article

(This article belongs to the Section Cancer Biology and Oncology)

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24 pages, 3582 KiB

Open AccessArticle

lncRNA EGOT Is the Marker of HPV Infection and a Prognostic Factor for HNSCC Patients

by Tomasz Kolenda, Piotr Białas, Kacper Guglas, Maciej Stasiak, Joanna Kozłowska-Masłoń, Karina Tylkowska, Anna Zapłata, Paulina Poter, Marlena Janiczek-Polewska, Patrycja Mantaj, Paulina Gieremek, Urszula Kazimierczak, Anna Przybyła, Katarzyna Regulska, Beata Stanisz, Ewa Leporowska, Andrzej Mackiewicz, Jacek Mackiewicz, Joanna Kazmierska, Zefiryn Cybulski and Anna Teresiak Show full author list Hide full author list

Biomedicines 2025, 13(4), 798; https://doi.org/10.3390/biomedicines13040798 (registering DOI) - 26 Mar 2025

Background: High-risk human papillomavirus (HPV) contributes to oropharyngeal cancers through mechanisms involving the deregulation of host cell functions by oncoproteins E6 and E7. Changes in the epigenome, particularly involving long non-coding RNAs (lncRNAs), are crucial for understanding HPV-related carcinogenesis. Methods: This study aimed [...] Read more.

Background: High-risk human papillomavirus (HPV) contributes to oropharyngeal cancers through mechanisms involving the deregulation of host cell functions by oncoproteins E6 and E7. Changes in the epigenome, particularly involving long non-coding RNAs (lncRNAs), are crucial for understanding HPV-related carcinogenesis. Methods: This study aimed to analyze the expression levels of lncRNAs in HPV-related head and neck squamous cell carcinoma (HNSCC) to determine their biological and clinical significance, addressing the current gap in clinically validated biomarkers for early screening and therapeutic interventions. Results: The study highlights the significant overexpression of the EGOT gene in HPV-positive HNSCC samples, suggesting its potential as a marker to distinguish between HPV-negative and HPV-positive cases. Furthermore, high EGOT expression correlates with better overall survival (OS) and indicates possible resistance to therapy, making it a valuable prognostic factor. Conclusions: These findings underscore the potential of incorporating EGOT expression analysis in clinical practice for improved patient stratification and treatment outcomes in HNSCC. Full article

(This article belongs to the Special Issue Advances in Head and Neck Cancer)

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12 pages, 855 KiB

Open AccessArticle

Comparative Analysis of Laboratory Markers, Severity Scores, and Outcomes in 179 Patients with Severe Acute Pancreatitis

by Tudorel Mihoc, Catalin Pirvu, Amadeus Dobrescu, Dan Brebu, Anca Monica Oprescu Macovei, Stelian Pantea, Claudia Borza, Patrick Dumitrescu and Monica Laura Cara

Biomedicines 2025, 13(4), 797; https://doi.org/10.3390/biomedicines13040797 (registering DOI) - 26 Mar 2025

Background and Objectives: Severe acute pancreatitis carries a substantial risk of complications and death. Prompt identification of prognostic factors is crucial to optimize management and reduce mortality. This study aims to compare inflammatory scores, laboratory markers, and clinical outcomes between survivors and [...] Read more.

Background and Objectives: Severe acute pancreatitis carries a substantial risk of complications and death. Prompt identification of prognostic factors is crucial to optimize management and reduce mortality. This study aims to compare inflammatory scores, laboratory markers, and clinical outcomes between survivors and non-survivors with severe acute pancreatitis, drawing on data from 179 patients admitted between 2017 and 2024. Methods: We conducted a retrospective cohort study of 179 patients diagnosed with severe acute pancreatitis. Of these, 55 patient records were extracted from an existing database, and an additional 124 were included from hospital archives (2017–2024). We divided participants into survivors (n = 121) and non-survivors (n = 58). Clinical data were obtained from medical records, including demographic information, comorbidities, laboratory markers (neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR)), and severity scores (Acute Physiology and Chronic Health Evaluation (APACHE), Computed Tomography Severity Index (CTSI), and Ranson). Results: Non-survivors had significantly higher ages (mean of 66.4 vs. 52.7 years, p = 0.002), elevated inflammatory markers (median NLR of 14.2 vs. 10.3, p = 0.031), and more frequent multiorgan failure (75.9% vs. 31.4%, p < 0.001). The timing of intervention before 28 days was associated with higher mortality (p = 0.004). Chronic kidney disease and advanced cardiovascular comorbidities independently predicted worse survival (p = 0.009). The mortality rate in this cohort was 32.4%. Logistic regression identified age >60 years with an odds ratio (OR = 2.9), multiple organ failure (OR = 4.1), and high severity scores as primary contributors to mortality. Conclusions: Advanced age, comorbidities, elevated inflammatory markers, and multiple organ failure significantly impact mortality in severe acute pancreatitis. Delaying major interventions when feasible, optimizing perioperative care, and early recognition of high-risk patients may improve outcomes. Further research should explore targeted management strategies for high-risk groups and refine the role of delayed or minimally invasive approaches in severe acute pancreatitis management. Full article

(This article belongs to the Section Molecular and Translational Medicine)

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16 pages, 4239 KiB

Open AccessArticle

Caveolin Scaffolding Domain (CSD) Peptide LTI-2355 Modulates the Phagocytic and Synthetic Activity of Lung-Derived Myeloid Cells in Idiopathic Pulmonary Fibrosis (IPF) and Post-Acute Sequelae of COVID Fibrosis (PASC-F)

by Brecht Creyns, BreAnne MacKenzie, Yago Amigo Pinho Jannini Sa, Ana Lucia Coelho, Dale Christensen, Tanyalak Parimon, Brian Windsor and Cory M. Hogaboam

Biomedicines 2025, 13(4), 796; https://doi.org/10.3390/biomedicines13040796 (registering DOI) - 26 Mar 2025

Rationale: The role of the innate immune system in idiopathic pulmonary fibrosis (IPF) remains poorly understood. However, a functional myeloid compartment is required to remove dying cells and cellular debris, as well as to mediate innate immune responses against pathogens. Aberrant macrophage [...] Read more.

Rationale: The role of the innate immune system in idiopathic pulmonary fibrosis (IPF) remains poorly understood. However, a functional myeloid compartment is required to remove dying cells and cellular debris, as well as to mediate innate immune responses against pathogens. Aberrant macrophage activity has been described in patients with post-acute sequelae of COVID fibrosis (PASC-F), and caveolin scaffolding domain (CSD) peptides have been found to attenuate inflammation and fibrosis in mouse lung injury models. Therefore, we examined, for the first time, the effects of CSD peptide LTI-2355 on the functional and synthetic properties of human myeloid cells isolated from lung explant tissue of donor lungs as well as IPF and PASC-F lung explant tissue. Methods and Results: CD45⁺ myeloid cells isolated from lung explant tissue from IPF and PASC-F patients exhibited an impaired capacity to clear autologous dead cells and cellular debris. The uptake of pathogen-coated bioparticles was impaired in myeloid cells from both fibrotic patient groups independent of the type of pathogen, highlighting an intrinsic functional cell impairment. LTI-2355 improved the phagocytic activity of both IPF and PASC-F myeloid cells, and this improvement was paired with decreased proinflammatory and pro-fibrotic synthetic activity. LTI-2355 was also shown to primarily target CD206-expressing IPF and PASC-F myeloid cells. Conclusions: Primary myeloid cells from IPF and PASC-F patients exhibit dysfunctional phagocytic and synthetic properties that are modulated by LTI-2355. LTI-2355 treatment of IPF myeloid cells resulted in significantly reduced sCD163, IFN-α2, IFN-γ, IL-2, IL-10, IL-12p40, and MMP-1 in the cell supernatant. This study highlights an additional mechanism of action of the CSD peptide in the treatment of IPF and progressive fibrotic lung disease. Full article

(This article belongs to the Special Issue The Molecular Basis of the Immune Response in Pulmonary Fibrosis)

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16 pages, 2630 KiB

Open AccessArticle

Introducing a Novel Personalized Microbiome-Based Treatment for Inflammatory Bowel Disease: Results from NostraBiome’s Internal Validation Study

by Adrian Goldiș, Radu Dragomir, Marina Adriana Mercioni, Christian Goldiș, Diana Sirca, Ileana Enatescu and Oana Belei

Biomedicines 2025, 13(4), 795; https://doi.org/10.3390/biomedicines13040795 (registering DOI) - 26 Mar 2025

Background/Objectives: Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn’s disease, is characterized by chronic gut inflammation driven by microbial dysbiosis and immune dysfunction. Current therapies primarily involve anti-inflammatory and immunomodulatory strategies; however, many patients experience an inadequate response or a gradual loss [...] Read more.

Background/Objectives: Inflammatory bowel disease (IBD), encompassing ulcerative colitis and Crohn’s disease, is characterized by chronic gut inflammation driven by microbial dysbiosis and immune dysfunction. Current therapies primarily involve anti-inflammatory and immunomodulatory strategies; however, many patients experience an inadequate response or a gradual loss of efficacy over time. This study evaluates the clinical efficacy of personalized microbiome modulation (PMM)—an AI-driven intervention designed to restore microbial balance and improve key treatment outcomes such as symptom control and remission rates. Methods: This was a single-arm, open-label validation trial involving 27 patients with moderate-to-severe IBD who had experienced prior treatment failure. Participants underwent three months of PMM, which included personalized dietary modifications, targeted probiotic supplementation, and antimicrobial interventions based on gut microbiome sequencing. Primary outcomes included stool frequency and consistency as well as inflammatory markers (C-reactive protein and fecal calprotectin), while secondary outcomes assessed nutritional status, metabolic function, and quality of life. Statistical analyses included paired t-tests and repeated measures ANOVA to determine significant changes over time. Results: PMM led to significant clinical improvements, including a 58% reduction in stool frequency (p < 0.001) and improved stool consistency. CRP and fecal calprotectin levels decreased markedly (p < 0.001), suggesting reduced systemic inflammation. Additionally, iron, vitamin B12, and vitamin D deficiencies improved (p < 0.001), alongside weight gain and increased energy levels. Notably, patients on anti-TNF biologics showed enhanced response rates, suggesting potential synergistic effects between microbiome modulation and biologic therapy. Conclusions: This study highlights PMM as a promising adjunctive therapy for IBD, demonstrating benefits across clinical, inflammatory, and metabolic parameters. While findings support the role of microbiome-targeted interventions in disease management, larger randomized controlled trials are required to confirm the long-term efficacy and applicability in broader patient populations. Full article

(This article belongs to the Special Issue Advanced Research of Gut Microbiota in Health and Diseases—2nd Edition)

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14 pages, 1098 KiB

Open AccessReview

The Role of STEAP1 in Prostate Cancer: Implications for Diagnosis and Therapeutic Strategies

by Lingling Zhang, Xinyi Ren, Ran An, Hongchen Song, Yaqi Tian, Xuan Wei, Mingjun Shi and Zhenchang Wang

Biomedicines 2025, 13(4), 794; https://doi.org/10.3390/biomedicines13040794 (registering DOI) - 26 Mar 2025

Prostate cancer (PCa) is one of the most common malignancies and the second leading cause of cancer-related death in men worldwide. The six-transmembrane epithelial antigen of the prostate 1 (STEAP1) is exceptionally overexpressed in PCa, maintaining high expression even in the castration-resistant prostate [...] Read more.

Prostate cancer (PCa) is one of the most common malignancies and the second leading cause of cancer-related death in men worldwide. The six-transmembrane epithelial antigen of the prostate 1 (STEAP1) is exceptionally overexpressed in PCa, maintaining high expression even in the castration-resistant prostate cancer (CRPC) stage, making it a promising target for diagnosis and treatment. STEAP1-positive extracellular vesicles and STEAP1-PET imaging are optimistic approaches for the non-invasive detection of different stages of PCa. STEAP1-targeted therapy includes an antibody–drug conjugate (ADC), chimeric antigen receptor T cell (CAR-T), T-cell engager (TCE), and vaccines, which demonstrate valuable therapeutic prospects. This review presents the structure and pathophysiological function of STEAP1, synthesizes cutting-edge advances in STEAP1-targeted molecular imaging and clinical applications, and critically analyzes their translational potential to overcome the limitations of current PCa diagnosis and treatment. Full article

(This article belongs to the Special Issue Urogenital Cancers: New Molecular and Translational Aspects on Carcinogenesis and Treatments)

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21 pages, 11005 KiB

Open AccessArticle

Synthesis and Evaluation of Isosteviol Derivatives: Promising Anticancer Therapies for Colon Cancer

by Yecang Chen, Feifei Zhu, Yuxin Ding, Lin Xing, Enxiao Wang, Yixiang Fang, Ruilong Sheng, Qidong Tu and Ruihua Guo

Biomedicines 2025, 13(4), 793; https://doi.org/10.3390/biomedicines13040793 (registering DOI) - 25 Mar 2025

Background: Isosteviol, a tetracyclic diterpenoid with a beyerene-type skeleton, exhibited wide pharmacological activities and an inhibitory impact on tumor proliferation in colon cancer; Methods: 22 isosteviol derivatives were synthesized by modifying the C-16 and C-19 position of isosteviol, and then the inhibitory activities [...] Read more.

Background: Isosteviol, a tetracyclic diterpenoid with a beyerene-type skeleton, exhibited wide pharmacological activities and an inhibitory impact on tumor proliferation in colon cancer; Methods: 22 isosteviol derivatives were synthesized by modifying the C-16 and C-19 position of isosteviol, and then the inhibitory activities of derivatives 2–22 were evaluated by CCK8 method. Next, the structure–activity relationships (SARs) of these isosteviol derivatives in HCT116 cells were discussed in detail. Network pharmacology was employed to predict and analyze the targets of isosteviol in the treatment of colon cancer; Results: The results indicated derivative 8 possessed stronger inhibitory activity against HCT116 and HepG2 cells (IC₅₀ = 6.20 ± 0.61 μM for HCT116, and IC₅₀ = 39.84 ± 0.43 μM for HepG2). Additionally, cell cycle analysis indicated that derivative 8 arrested HCT116 cells at the G1 phase and increased the percentage of apoptotic cells. Moreover, the molecular docking showed that derivative 8 could interact with TP53 through its Tyr-1600 and Leu-1534 residues (docking energy: −11.84 kcal/mol); Conclusions: With these results, we can conclude that derivative 8 may be a promising candidate for anticancer chemotherapy. Full article

(This article belongs to the Special Issue Compounds from Natural Products as Sources for Drug Discovery)

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22 pages, 10224 KiB

Open AccessArticle

Centromere Protein F Is a Potential Prognostic Biomarker and Target for Cutaneous Melanoma

by Lilu Xie, Kangjie Shen, Chenlu Wei, Jiangying Xuan, Jiayi Huang, Zixu Gao, Ming Ren, Lu Wang, Yu Zhu, Shaoluan Zheng, Chuanyuan Wei and Jianying Gu

Biomedicines 2025, 13(4), 792; https://doi.org/10.3390/biomedicines13040792 - 25 Mar 2025

Background/Objectives: Cutaneous melanoma (CM) is a highly aggressive malignancy with poor prognosis, necessitating novel biomarkers and therapeutic targets. Centromere protein F (CENPF), a mitotic regulator, has been implicated in tumor progression, but its role in melanoma remains unclear. This study aimed to investigate [...] Read more.

Background/Objectives: Cutaneous melanoma (CM) is a highly aggressive malignancy with poor prognosis, necessitating novel biomarkers and therapeutic targets. Centromere protein F (CENPF), a mitotic regulator, has been implicated in tumor progression, but its role in melanoma remains unclear. This study aimed to investigate the clinical significance, biological function, and regulatory mechanisms of CENPF in melanoma. Methods: Public melanoma datasets (GSE46517, GSE3189, and GSE7553) were re-analyzed to identify differentially expressed genes (DEGs). CENPF expression was validated in clinical samples (n = 128), melanoma cell lines, and xenograft models. Functional assays (EdU, CCK-8, colony formation, wound healing, transwell, and flow cytometry) and bioinformatics analyses (GO, KEGG, GSEA, and SCENIC) were performed to assess proliferation, apoptosis, metastasis, and regulatory pathways. In vivo tumorigenesis and metastasis were evaluated in BALB/c nude mice. Results: CENPF was significantly upregulated in melanoma tissues and cell lines compared to controls (p < 0.05). High CENPF expression correlated with advanced Clark level (p = 0.006), ulceration (p = 0.04), and poor overall survival (p = 0.005). Knockdown of CENPF suppressed melanoma cell proliferation, migration, and invasion in vitro, while inducing G2/M phase arrest and apoptosis. In vivo, CENPF silencing reduced tumor growth and lung metastasis. Mechanistically, CENPF was transcriptionally activated by E2F3, and the E2F3-CENPF axis promoted cell cycle progression via G2/M checkpoint activation and P53 pathway suppression. Conclusions: CENPF serves as a prognostic biomarker and therapeutic target in melanoma. Its upregulation drives tumor progression through cell cycle dysregulation and immune evasion, while targeting the E2F3-CENPF axis may offer a novel strategy for melanoma treatment. These findings provide critical insights into melanoma pathogenesis and potential clinical applications. Full article

(This article belongs to the Special Issue Targeting Transcription Factors and Oncogenic Proteins for Cancer Therapy (2nd Edition))

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23 pages, 1947 KiB

Open AccessReview

Microbiome and Postbiotics in Skin Health

by Santosh Kumar Prajapati, Lalitha Lekkala, Dhananjay Yadav, Shalini Jain and Hariom Yadav

Biomedicines 2025, 13(4), 791; https://doi.org/10.3390/biomedicines13040791 - 25 Mar 2025

The skin microbiome, a diverse and dynamic ecosystem of microorganisms, plays a pivotal role in maintaining skin health by interacting with skin cells, immune components, and structural barriers. It is essential for skin homeostasis, immune defense, and protection against pathogenic colonization. Dysbiosis in [...] Read more.

The skin microbiome, a diverse and dynamic ecosystem of microorganisms, plays a pivotal role in maintaining skin health by interacting with skin cells, immune components, and structural barriers. It is essential for skin homeostasis, immune defense, and protection against pathogenic colonization. Dysbiosis in the microbiome has been implicated in numerous dermatological conditions, including acne, eczema, psoriasis, and rosacea. Acne, the most prevalent skin condition, affects up to 85% of individuals at some point in their lives, while eczema and psoriasis impose significant public health and economic burdens. The composition of the skin microbiome varies across skin types and anatomical sites, with sebaceous, moist, and dry areas fostering distinct microbial communities. Emerging therapeutic strategies such as microbiome-targeted treatments offer novel avenues for addressing skin diseases. Among these approaches, postbiotics have gained significant attention for their safety and efficacy. Unlike probiotics, postbiotics are non-viable microbial cells or their metabolites, which reduce safety concerns while providing functional benefits such as UV protection and wound healing. This review consolidates current insights into the role of the skin microbiome in health and disease, emphasizing postbiotics as a promising therapeutic strategy by exploring the clinical and commercial potential of microbiome-based treatments, particularly postbiotics, and their ability to redefine dermatological care and improve patient outcomes. Full article

(This article belongs to the Special Issue Wound Healing: From Basic to Clinical Research)

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16 pages, 1331 KiB

Open AccessReview

Emerging Pharmacological Approaches for the Treatment of Arterial Hypertension

by Francesca Schinzari, Rossella Montenero, Carmine Cardillo and Manfredi Tesauro

Biomedicines 2025, 13(4), 790; https://doi.org/10.3390/biomedicines13040790 - 25 Mar 2025

Despite the availability of several drug classes for the treatment of hypertension, the current approaches to high blood pressure (BP) are not fully satisfying the needs of this patient population. As a result, in recent years, many clinical trials have investigated novel pharmacological [...] Read more.

Despite the availability of several drug classes for the treatment of hypertension, the current approaches to high blood pressure (BP) are not fully satisfying the needs of this patient population. As a result, in recent years, many clinical trials have investigated novel pharmacological approaches for lowering high BP. As overactivity of the renin–angiotensin–aldosterone system is often present in hypertensive patients, especially those with resistant hypertension, several studies have focused on novel strategies to counteract this phenomenon by the use of non-steroidal inhibitors of the mineralocorticoid receptors, aldosterone synthase inhibitors or RNA-targeting therapies to inhibit the hepatic synthesis of angiotensinogen. The latter approach in particular might offer the additional advantage of reducing the daily pill burden of these patients, hence mitigating the common occurrence of non-adherence to treatment. Because obesity and diabetes are common risk factors for hypertension (a high percentage of individuals with resistant hypertension being obese), numerous investigations have analyzed the BP-lowering effects of those agents, such as glucagon-like peptide-1 receptor agonists and sodium–glucose co-transporter-2 inhibitors, which have been shown to reduce body weight and improve cardiovascular outcomes in these patients. Available evidence suggests that these drug classes can indeed afford a clinically meaningful BP decrease and, potentially, reduce the treatment burden. In conclusion, even though the rates of uncontrolled hypertension remain high, several novel therapeutic options are in the offing. As these emerging treatments will compound with many already available agents, future efforts should be directed at better phenotyping patients to tailor the most suitable approach for each one. Full article

(This article belongs to the Section Endocrinology and Metabolism Research)

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