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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 - Q1 (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

28 pages, 27668 KiB

Open AccessArticle

An Explainable Fuzzy Framework for Assessing Preeclampsia Classification

by Matías Salinas, Daira Velandia, Leondry Mayeta-Revilla, Ayleen Bertini, Marvin Querales, Fabian Pardo and Rodrigo Salas

Biomedicines 2025, 13(6), 1483; https://doi.org/10.3390/biomedicines13061483 (registering DOI) - 16 Jun 2025

Background: Preeclampsia remains a leading cause of maternal morbidity worldwide. There is a critical need for predictive systems that not only perform accurately but also provide interpretable insights for clinical decision-making. This work introduces SK-MOEFS, an explainable framework based on fuzzy logic and [...] Read more.

Background: Preeclampsia remains a leading cause of maternal morbidity worldwide. There is a critical need for predictive systems that not only perform accurately but also provide interpretable insights for clinical decision-making. This work introduces SK-MOEFS, an explainable framework based on fuzzy logic and multi-objective evolutionary optimization, designed to classify preeclampsia risk while generating clinically interpretable rules. Methods: The model integrates fuzzy decision trees with a genetic algorithm to identify a compact and relevant set of rules, optimized for both accuracy and interpretability. The system was trained and evaluated on third-trimester pregnancy data from a publicly available, multi-ethnic cohort comprising 574 individuals. All processes, including preprocessing, training, and evaluation, were conducted using open-source tools, ensuring reproducibility. Results: SK-MOEFS achieved 91% classification accuracy, an AUC of 0.89, and a recall of 0.88—outperforming other standard interpretable models while maintaining high transparency. The model emphasizes minimizing false negatives, which is critical in clinical risk stratification for preeclampsia. Conclusions: Beyond predictive performance, SK-MOEFS offers a rule translation and defuzzification layer that outputs probabilistic interpretations in natural language, enhancing its suitability for clinical use. This framework provides an effective bridge between algorithmic inference and human clinical judgment, supporting transparent and reliable decision-making in maternal care. Full article

(This article belongs to the Special Issue Advanced Research in Early Pregnancy Loss and Other Pregnancy Complications)

30 pages, 1777 KiB

Open AccessReview

Post-COVID Metabolic Fallout: A Growing Threat of New-Onset and Exacerbated Diabetes

by Shaghayegh Hemat Jouy, Harry Tonchev, Sarah M. Mostafa and Abeer M. Mahmoud

Biomedicines 2025, 13(6), 1482; https://doi.org/10.3390/biomedicines13061482 (registering DOI) - 16 Jun 2025

Emerging evidence highlights the profound and lasting impact of severe illnesses such as COVID-19, particularly among individuals with underlying comorbidities. Patients with pre-existing conditions like diabetes mellitus (DM) are disproportionately affected, facing heightened risks of both disease exacerbation and the onset of new [...] Read more.

Emerging evidence highlights the profound and lasting impact of severe illnesses such as COVID-19, particularly among individuals with underlying comorbidities. Patients with pre-existing conditions like diabetes mellitus (DM) are disproportionately affected, facing heightened risks of both disease exacerbation and the onset of new complications. Notably, the convergence of advanced age and DM has been consistently associated with poor COVID-19 outcomes. However, the long-term metabolic consequences of SARS-CoV-2 infection, especially its role in disrupting glucose homeostasis and potentially triggering or worsening DM, remain incompletely understood. This review synthesizes current clinical and experimental findings to clarify the bidirectional relationship between COVID-19 and diabetes. We critically examine literature reporting deterioration of glycemic control, onset of hyperglycemia in previously non-diabetic individuals, and worsening of metabolic parameters in diabetic patients after infection. Furthermore, we explore proposed mechanistic pathways, including pancreatic β-cell dysfunction, systemic inflammation, and immune-mediated damage, that may underpin the development or progression of DM in the post-COVID setting. Collectively, this work underscores the urgent need for continued research and clinical vigilance in managing metabolic health in COVID-19 survivors. Full article

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

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31 pages, 1785 KiB

Open AccessReview

Chemerin as a Driver of Cardiovascular Diseases: New Perspectives and Future Directions

by Anna M. Imiela, Jan Stępnicki, Patrycja Sandra Zawadzka, Angelika Bursa and Piotr Pruszczyk

Biomedicines 2025, 13(6), 1481; https://doi.org/10.3390/biomedicines13061481 - 16 Jun 2025

In recent years, the immune system has emerged as a key player in the development of atherosclerosis, heart failure, venous thromboembolism, and systemic hypertension. Obesity and related cardiovascular diseases (CVDs) remain the leading global cause of death. Adipokines—hormones produced by adipose tissue—exert diverse [...] Read more.

In recent years, the immune system has emerged as a key player in the development of atherosclerosis, heart failure, venous thromboembolism, and systemic hypertension. Obesity and related cardiovascular diseases (CVDs) remain the leading global cause of death. Adipokines—hormones produced by adipose tissue—exert diverse endocrine and immunomodulatory effects. Among them, chemerin, discovered in the early 20th century, is a chemotactic molecule that recruits dendritic cells, endothelial cells, macrophages, and lymphocytes during early immune responses. It regulates cell migration and vascular homeostasis. Dysregulated adipokine profiles contribute to chronic inflammation, insulin resistance, metabolic syndrome, and impaired blood pressure control. This review explores chemerin’s potential role in CVD pathogenesis, focusing on its immunomodulatory functions, impact on vascular inflammation, and endothelial dysfunction. The presented work also examines recent findings on chemerin’s diagnostic and therapeutic potential in cardiovascular health. Full article

(This article belongs to the Special Issue The Role of Chemerin in Human Disease—2nd Edition)

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16 pages, 1850 KiB

Open AccessArticle

Immune System Alterations in the Development of Three Urological Cancers: Insights from Large-Sample Mendelian Randomization

by Zhijian Chen, Ye Xie, Xiong Chen, Guibin Hong, Runnan Shen, Haishan Lin, Fan Jiang, Yun Wang, Mengyi Zhu, Yixuan Liu, Haoxuan Wang, Hongkun Yang, Tianxin Lin and Shaoxu Wu

Biomedicines 2025, 13(6), 1480; https://doi.org/10.3390/biomedicines13061480 - 16 Jun 2025

Background: Urological cancers (UCs) greatly impact global public health. While immunity plays an important role, the contribution of specific immune cell traits to the development of UCs remains unclear. In our study, we employed Mendelian randomization (MR) to elucidate the causal relationship between [...] Read more.

Background: Urological cancers (UCs) greatly impact global public health. While immunity plays an important role, the contribution of specific immune cell traits to the development of UCs remains unclear. In our study, we employed Mendelian randomization (MR) to elucidate the causal relationship between 731 immune cell traits and three common UCs, namely kidney cancer (KC), bladder cancer (BC), and prostate cancer (PC). Methods: In our research, we adopted and preprocessed the statistics of 731 immune cell types from the GWAS Catalog. The data of three common UCs were acquired from two databases, FinnGen and IEU. Five MR analysis models, including random-effect inverse-variance weighted, weighted median, MR Egger, weighted mode, and simple mode, were used to assess the association between 731 immune cell traits and UCs. Subsequently, a meta-analysis of the IVW method was performed, and the significant results were analyzed using the reverse MR method. Sensitivity analyses, including leave-one-out analysis, were also performed. Results: When analyzing the two datasets separately, 25, 41, and 23 immune phenotypes were found to be significantly associated with BC, PC, and KC, respectively. When applying meta-analysis, the combined results showed that a total of 18 immune cell types manifested the significant association, including 4 and 14 immune cell traits regarding BC and PC, respectively. Utilizing reverse MR analysis on the combined results, we found that two immune cell traits, namely lymphocyte absolute cell counts and CX3CR1 on CD14+ CD16- monocytes, showed a reverse causal relationship with PC. Conclusions: Our research depicts the immune landscape for these three common UCs, highlighting their strong genetic associations with immune cells. It provides valuable insights for identifying the systemic immunological context of cancer susceptibility and the development of blood-based immunological biomarkers and therapeutic targets. Full article

(This article belongs to the Special Issue Advanced Research on Genitourinary Cancer)

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12 pages, 1031 KiB

Open AccessArticle

IDH1 Mutation Impacts DNA Repair Through ALKBH2 Rendering Glioblastoma Cells Sensitive to Artesunate

by Olivier Switzeny, Stefan Pusch, Markus Christmann and Bernd Kaina

Biomedicines 2025, 13(6), 1479; https://doi.org/10.3390/biomedicines13061479 - 16 Jun 2025

Background: Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are enzymes that catalyze the oxidative decarboxylation of isocitrate to alpha-ketoglutarate (α-KG), which is essential for many metabolic processes, including some steps in DNA repair. In tumors, notably in gliomas, IDH1 and IDH2 [...] Read more.

Background: Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are enzymes that catalyze the oxidative decarboxylation of isocitrate to alpha-ketoglutarate (α-KG), which is essential for many metabolic processes, including some steps in DNA repair. In tumors, notably in gliomas, IDH1 and IDH2 are frequently mutated. The mutation found in different cancers is functionally active, causing, instead of α-KG, the formation of 2-hydroxyglutarate (2-HG), which inhibits α-KG-dependent enzymes. Gliomas harboring mutated IDH1/2 show a better prognosis than IDH1 wild-type (wt) tumors of the same grade, which might result from the inhibition of DNA repair functions. A DNA repair enzyme dependent on α-KG is alkB homolog 2 (ALKBH2), which removes several lesions from DNA. These findings prompted us to investigate the response of glioma cells to artesunate (ART), a plant ingredient with genotoxic and anticancer activity currently used in several trials. Materials and Methods: We used isogenic glioblastoma cell lines that express IDH1 wild-type or, based on a TET-inducible system, the IDH1 mutant (mt) protein, and treated them with increasing doses of artesunate. We also treated glioblastoma cells with 2-HG, generated ALKBH2 knockout cells, and checked their sensitivity to the cytotoxic effects of artesunate. Results: We show that the cell-killing effect of ART is enhanced if the IDH1 mutant (R132H) is expressed in glioblastoma cells. Further, we show that 2-HG imitates the effect of IDH1mt as 2-HG ameliorates the cytotoxicity of ART. Finally, we demonstrate that the knockout of ALKBH2 causes the sensitization of glioblastoma cells to ART. Conclusions: The data indicate that ALKBH2 protects against the anticancer effect of ART, and the mutation of IDH1/2 commonly occurring in low-grade gliomas sensitizes to ART via an ALKBH2-dependent mechanism. The data support the use of ART in the therapy of IDH1/2-mutated cancers both in combination with chemotherapy and adjuvant treatment. Full article

(This article belongs to the Special Issue Glioma Therapy: Current Status and Future Prospects)

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14 pages, 779 KiB

Open AccessReview

Macrolide Antibiotic Mediated Cardiac Arrhythmias: Emerging Concepts and Clinical Implications

by Fatima Iqbal, Alyssa Derouen, Robin Ren, Adam M. Kaye, Shahab Ahmadzadeh, Sahar Shekoohi and Alan D. Kaye

Biomedicines 2025, 13(6), 1478; https://doi.org/10.3390/biomedicines13061478 - 16 Jun 2025

The macrolide class of antibiotics are widely utilized in clinical settings for a broad range of bacterial infections and have additional roles as immunomodulatory agents. Although efficacious with a good safety profile overall, they have been associated with prolongation of the QT interval [...] Read more.

The macrolide class of antibiotics are widely utilized in clinical settings for a broad range of bacterial infections and have additional roles as immunomodulatory agents. Although efficacious with a good safety profile overall, they have been associated with prolongation of the QT interval and development of the polymorphic ventricular tachycardia, Torsades de pointes (TdP). In a 2020 scientific statement, the American Heart Association (AHA) classified azithromycin, clarithromycin and erythromycin as QT-prolonging drugs known to cause TdP and the online database, CredibleMeds, that maintains a list of drugs known to cause QT prolongation classifies these drugs as having an increased risk of QT prolongation. The mechanism of this risk has been delineated to involve macrolide binding to and a blockade of delayed rectifier potassium channels that conduct rapid potassium current, I_kr, during repolarization, leading to prolonged repolarization and subsequent QT prolongation. Studies investigating this association have revealed variable results, with several suggesting that the risk of QT prolongation and TdP with macrolide use may be highly dependent on underlying patient risk factors and comorbidities. In the present investigation, we summarize current evidence on association of macrolide antibiotics, azithromycin, clarithromycin and erythromycin, with the development of QT prolongation and TdP, pathophysiology of and risk factors predisposing to development of these events, the role of implementation of strategies to reduce this risk and highlight emerging research. Full article

(This article belongs to the Special Issue Pathogenesis, Diagnosis and Treatment of Cardiomyopathy and Cardiac Arrhythmias (2nd Edition))

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17 pages, 3218 KiB

Open AccessArticle

Introducing a Novel Paper Point Method for Isolated Apical Sampling—The Controlled Apical Sampling Device: A Methodological Study

by Christoph Matthias Schoppmeier, Gustav Leo Classen, Silvia Contini, Paul Rebmann, David Brendlen, Michael Jochen Wicht and Anna Greta Barbe

Biomedicines 2025, 13(6), 1477; https://doi.org/10.3390/biomedicines13061477 - 15 Jun 2025

Objectives: To introduce a novel method for apical lesion sampling using a protected paper point device and to evaluate its effectiveness and robustness during the sampling process in vitro. Methods: A prototype for apical sample collection was developed as an adaptation [...] Read more.

Objectives: To introduce a novel method for apical lesion sampling using a protected paper point device and to evaluate its effectiveness and robustness during the sampling process in vitro. Methods: A prototype for apical sample collection was developed as an adaptation of the Micro-Apical Placement System—the device features a highly tapered screw head with a thin, hollow, stainless-steel tube and an internal wire piston. Standardized 5 mm paper points (ISO 0; PD Dental, Switzerland) served as carrier material. The prototype was tested using 30 × 3D-printed, single-rooted tooth models inoculated using two bacterial strains (Staphylococcus epidermidis and Escherichia coli) to simulate apical and intraradicular bacterial infections, respectively. The sampling process involved collecting and analyzing samples at specific timepoints, focusing on the presence or absence of E. coli contamination. Following sample collection, cultural detection of bacterial presence was performed by incubating the samples on agar plates to confirm the presence of E. coli. Samples were collected as follows: S0 (sterility control of the prototype), P0 (sterility control of the tooth model), P1 (apical sample collected with the CAPS (controlled apical sampling) device, and P2 (contamination control sample to check for the presence of E. coli inside the root canal). Results: Handling of the CAPS prototype was straightforward and reproducible. No loss of paper points or complications were observed during sample collection. All sterility samples (P0, S0) were negative for tested microorganisms, confirming the sterility of the setup. P2 samples confirmed the presence of E. coli in the root canal in all trials. The P1 samples were free from contamination in 86.67% of trials. Conclusions: The CAPS method for apical sampling demonstrated advances in the successful and precise sample collection of apically located S. epidermidis and will be a useful tool for endodontic microbiological analysis. Its user-friendly design and consistent performance highlight its potential for clinical application, contributing to more accurate microbial diagnostics and later patient-specific therapeutic approaches in endodontic treatments. Full article

(This article belongs to the Special Issue Feature Reviews in Biomaterials for Oral Diseases)

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16 pages, 715 KiB

Open AccessArticle

Effects of Methionine and Glutathione on Acute Ototoxicity Induced by Amikacin and Furosemide in an Animal Model of Hearing Threshold Decrease

by Marek Zadrożniak, Marcin Szymański and Jarogniew J. Luszczki

Biomedicines 2025, 13(6), 1476; https://doi.org/10.3390/biomedicines13061476 - 15 Jun 2025

Background/Objectives: Aminoglycoside antibiotics and loop diuretics are still the main causes of hearing loss in patients, and no specific prevention is available for this drug-induced ototoxicity. The aim of this study was to compare the protective effects of methionine (MET) and glutathione (GLUT) [...] Read more.

Background/Objectives: Aminoglycoside antibiotics and loop diuretics are still the main causes of hearing loss in patients, and no specific prevention is available for this drug-induced ototoxicity. The aim of this study was to compare the protective effects of methionine (MET) and glutathione (GLUT) in terms of the reduction in ototoxicity induced by mixtures of amikacin (AMI, an aminoglycoside antibiotic) and furosemide (FUR, a loop diuretic) in a mouse model in which the hearing threshold decreased by 20% and 50%, respectively. Methods: To compare the otoprotective effects of MET and GLUT on AMI- and FUR-induced ototoxicity in mice, an isobolographic transformation of interactions was applied. Results: MET, but not GLUT, mitigated the AMI- and FUR-induced hearing threshold changes in mice. Additionally, MET exerted an antagonistic interaction with a combination of FUR+AMI, as the hearing threshold decreased by 50%, and an additive interaction, with a tendency toward antagonism in the model of hearing threshold decreased by 20%. In contrast, GLUT exerted only additive interactions when combined with FUR+AMI for both variant hearing thresholds decreased by 20% and 50%, respectively. Only MET could be a potential otoprotective drug in further prevention of hearing loss induced by AMI and FUR. Conclusions: MET is superior to GLUT in mitigating AMI- and FUR-induced hearing threshold decreases in mice. MET could be recommended as an otoprotectant in the prevention of hearing loss in patients receiving AMI and FUR. Full article

(This article belongs to the Section Drug Discovery, Development and Delivery)

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14 pages, 762 KiB

Open AccessArticle

Combined Effects of Obstructive Sleep Apnea and Sleep Duration on Hypertension in Korean Adults: A Nationwide Study

by Seo Young Kang and Yunmi Kim

Biomedicines 2025, 13(6), 1475; https://doi.org/10.3390/biomedicines13061475 - 15 Jun 2025

Background: Obstructive sleep apnea (OSA) and abnormal sleep duration are known risk factors for hypertension. However, evidence regarding their combined effect on hypertension is limited and inconsistent. This study aimed to examine the independent and interactive associations of OSA risk and sleep duration [...] Read more.

Background: Obstructive sleep apnea (OSA) and abnormal sleep duration are known risk factors for hypertension. However, evidence regarding their combined effect on hypertension is limited and inconsistent. This study aimed to examine the independent and interactive associations of OSA risk and sleep duration with hypertension in Korean adults. Methods: We analyzed data from 14,579 adults aged ≥40 years who participated in the 2019–2022 Korea National Health and Nutrition Examination Survey. OSA risk was assessed using the STOP-Bang questionnaire and classified as low (0–2), moderate (3–4), or high (5–8). Sleep duration was self-reported and categorized as <6, 6–<7, 7–<8, 8–<9, and ≥9 h. Hypertension was defined based on measured blood pressure and antihypertensive medication use. Multivariate logistic regression was conducted to evaluate the associations. Results: A dose–response association was observed between OSA risk and hypertension prevalence: adjusted ORs (95 CIs) were 9.69 (8.37–11.23) for moderate and 36.58 (29.35–45.59) for high OSA risk. Sleep duration alone was not significantly associated with hypertension. However, interaction models showed a U-shaped relationship, with the lowest hypertension prevalence in those sleeping 7–<8 h. Among participants with high OSA risk, both short (<7 h) and long (≥9 h) sleep durations were associated with significantly higher hypertension risk (OR 48.49, 95% CI 19.68–119.50 for ≥9 h). Conclusions: OSA risk and sleep duration jointly affect hypertension risk. Individuals with high OSA risk who are short or long sleepers may require targeted interventions to improve blood pressure control. Full article

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

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12 pages, 602 KiB

Open AccessArticle

Effects of SGLT2 Inhibitors on Sleep Apnea Parameters and Cheyne–Stokes Respiration in Patients with Acute Decompensated Heart Failure: A Prospective Cohort Study

by Petar Kalaydzhiev, Tsvetelina Velikova, Yanitsa Davidkova, Gergana Voynova, Angelina Borizanova, Natalia Spasova, Neli Georgieva, Radostina Ilieva, Elena Kinova and Assen Goudev

Biomedicines 2025, 13(6), 1474; https://doi.org/10.3390/biomedicines13061474 - 14 Jun 2025

Background: Sleep-disordered breathing (SDB), particularly Cheyne–Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal [...] Read more.

Background: Sleep-disordered breathing (SDB), particularly Cheyne–Stokes respiration (CSR), is highly prevalent among patients hospitalized with acute decompensated heart failure (ADHF) and is associated with worse clinical outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) have demonstrated cardiorenal benefits in heart failure, but their effects on nocturnal respiratory parameters remain underexplored. Objectives: This study aims to evaluate the impact of SGLT2i therapy on key respiratory and cardiac indices including CSR burden, oxygenation, and right heart function in patients with ADHF and reduced left ventricular ejection fraction. Methods: In this single-center prospective cohort study, 60 patients with ADHF, LVEF < 40%, and a baseline apnea–hypopnea index (AHI) > 5 were assessed before and three months after the initiation of SGLT2i therapy. Sleep respiratory parameters were measured using home polygraphy (ApneaLink^TM), while cardiac and renal indices were evaluated by echocardiography, NT-proBNP, and the estimated glomerular filtration rate (eGFR). Structural and functional echocardiographic changes were analyzed both at baseline and following the 3-month treatment period. Patient-reported outcomes were assessed using the Epworth Sleepiness Scale (ESS) and Kansas City Cardiomyopathy Questionnaire (KCCQ). Results: After 3 months of SGLT2i therapy, significant improvements were observed in daytime sleepiness (ESS: −2.68 points; p < 0.001), CSR index (−5.63 events/h; p < 0.001), AHI (−3.07 events/h; p < 0.001), ODI (−6.11 events/h; p < 0.001), and mean nocturnal SpO₂ (+1.95%; p < 0.001). KCCQ scores increased by 9.16 points (p < 0.001), indicating improved quality of life. Cardiac assessments revealed reductions in NT-proBNP (−329.6 pg/mL; p < 0.001) and E/e′ ratio (−1.08; p < 0.001), with no significant change in LVEF or chamber dimensions. Right ventricular function improved, as evidenced by the increased TAPSE/sPAP ratio (+0.018; p < 0.001). Renal function remained stable, with a non-significant upward trend in eGFR. Conclusions: This exploratory study suggests that SGLT2 inhibitors may be associated with the attenuation of Cheyne–Stokes respiration and an improvement in right heart function in patients with ADHF, warranting further investigation in controlled trials. These findings highlight the potential of SGLT2is to address overlapping cardio-respiratory dysfunction in this high-risk population. Full article

(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 2nd Edition)

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29 pages, 2018 KiB

Open AccessReview

Neutrophil Spatiotemporal Regulatory Networks: Dual Roles in Tumor Growth Regulation and Metastasis

by Pengcheng Li, Feimu Fan, Bixiang Zhang, Chaoyi Yuan and Huifang Liang

Biomedicines 2025, 13(6), 1473; https://doi.org/10.3390/biomedicines13061473 - 14 Jun 2025

Neutrophils, accounting for 50–70% of circulating leukocytes, exhibit remarkable plasticity in tumor biology. Depending on tumor type and microenvironmental cues, they can exert either anti-tumor or pro-tumor effects. During tumor initiation, neutrophils exposed to chronic inflammation secrete cytokines and oncogenic microRNAs that promote [...] Read more.

Neutrophils, accounting for 50–70% of circulating leukocytes, exhibit remarkable plasticity in tumor biology. Depending on tumor type and microenvironmental cues, they can exert either anti-tumor or pro-tumor effects. During tumor initiation, neutrophils exposed to chronic inflammation secrete cytokines and oncogenic microRNAs that promote genomic instability and malignant transformation. In tumor progression, neutrophils adopt context-dependent phenotypes and execute diverse functions, including polarization into anti-tumor (N1) or pro-tumor (N2) subsets; secretion of inflammatory and angiogenic mediators; formation of neutrophil extracellular traps (NETs); production of reactive oxygen and nitrogen species (e.g., H₂O₂ and nitric oxide); and modulation of immune cell infiltration and function within the tumor microenvironment. During metastasis, neutrophils facilitate cancer dissemination through three principal mechanisms: (1) promoting epithelial–mesenchymal transition (EMT) via inflammatory signaling, adhesion molecule interactions, and lipid metabolic support; (2) establishing pre-metastatic niches by remodeling distant organ stroma through NETs and matrix metalloproteinases; and (3) reactivating dormant tumor cells in response to chronic inflammation, viral infection, or stress hormones. Collectively, neutrophils function as central regulators across all stages of tumor evolution, influencing cancer growth, immune evasion, and metastatic progression. This review aims to provide a comprehensive synthesis of neutrophil-mediated mechanisms in the tumor microenvironment and highlight emerging strategies for neutrophil-targeted cancer therapy. Full article

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

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17 pages, 2085 KiB

Open AccessReview

What to Aspect from DCB PCI in Different Plaque Morphologies?

by Flavius-Alexandru Gherasie, Raluca Ciomag (Ianula) and Luana-Maria Gherasie

Biomedicines 2025, 13(6), 1472; https://doi.org/10.3390/biomedicines13061472 - 14 Jun 2025

The evolution of percutaneous coronary intervention (PCI) has led to significant advances in drug-coated balloon (DCB) technology, offering a stent-free alternative for treating coronary artery disease. While paclitaxel-coated balloons (PCBs) have been the standard, sirolimus-coated balloons (SCBs) are emerging as a viable alternative [...] Read more.

The evolution of percutaneous coronary intervention (PCI) has led to significant advances in drug-coated balloon (DCB) technology, offering a stent-free alternative for treating coronary artery disease. While paclitaxel-coated balloons (PCBs) have been the standard, sirolimus-coated balloons (SCBs) are emerging as a viable alternative with distinct pharmacokinetic and clinical benefits. This review explores the mechanisms of action of paclitaxel and sirolimus, their impact on different plaque morphologies, and the clinical implications of DCB selection. Paclitaxel facilitates positive vascular remodeling and is particularly effective in fibrotic and lipid-rich plaques, but its poor penetration in calcified lesions remains a limitation. Sirolimus, with its homogeneous tissue distribution and anti-inflammatory properties, is better suited for unstable, lipid-rich, and inflammatory plaques, where it promotes plaque stabilization. Recent randomized trials and meta-analyses have compared SCBs vs. PCBs in both de novo lesions and in-stent restenosis, showing non-inferior outcomes. Additionally, DCBs demonstrate comparable efficacy to DES in small vessel disease, reducing the need for permanent metallic scaffolds. This review summarizes the current evidence on DCB selection based on plaque characteristics and highlights areas for further investigation in personalized PCI strategies. Given the narrative review design, the authors conducted a comprehensive literature search using databases such as PubMed and MEDLINE. Keywords included “drug-coated balloon”, “paclitaxel-coated balloon”, “sirolimus-coated balloon”, “in-stent restenosis”, and “plaque morphology”. Studies were selected based on relevance, including randomized controlled trials, registries, and meta-analyses. No formal inclusion/exclusion criteria or systematic screening were applied due to the nature of narrative synthesis. Full article

(This article belongs to the Special Issue Progress in Cardiovascular Pharmacology)

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16 pages, 2420 KiB

Open AccessReview

Applications of Surface Plasmon Resonance in Heparan Sulfate Interactome Research

by Payel Datta, Jonathan S. Dordick and Fuming Zhang

Biomedicines 2025, 13(6), 1471; https://doi.org/10.3390/biomedicines13061471 - 14 Jun 2025

Surface plasmon resonance (SPR) is a powerful tool for analyzing biomolecular interactions and is widely used in basic biomedical research and drug discovery. Heparan sulfate (HS) is a linear complex polysaccharide and a key component of the extracellular matrix and cell surfaces. HS [...] Read more.

Surface plasmon resonance (SPR) is a powerful tool for analyzing biomolecular interactions and is widely used in basic biomedical research and drug discovery. Heparan sulfate (HS) is a linear complex polysaccharide and a key component of the extracellular matrix and cell surfaces. HS plays a pivotal role in maintaining cellular functions and tissue homeostasis by interacting with numerous proteins, making it essential for normal physiological processes and disease states. Deciphering the interactome of HS unlocks the mechanisms underlying its biological functions and the potential for novel HS-related therapeutics. This review presents an overview of the recent advances in the application of SPR technology to HS interactome research. We discuss methodological developments, emerging trends, and key findings that illustrate how SPR is expanding our knowledge of HS-mediated molecular interactions. Additionally, we highlight the potential of SPR-based approaches in identifying novel therapeutic targets and developing HS-mimetic drugs, thereby opening new avenues for intervention in HS-related diseases. Full article

(This article belongs to the Special Issue Advances in Heparan Sulfate Biology: Protein Interactions and Therapeutic Implications)

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22 pages, 2850 KiB

Open AccessSystematic Review

Polymer-Free Versus Biodegradable Polymer Drug-Eluting Stents in Coronary Artery Disease: Updated Systematic Review and Meta-Analysis of Clinical, Angiographic, and OCT Outcomes

by Marcello Marchetta, Stefano Sasso, Vincenzo Paragliola, Andrea Giovanni Parato, Diego De Angelis, Giulio Russo, Giovanni Albano, Daniela Benedetto, Federico Moretti, Francesco Valenti, Gianluca Massaro, Gaetano Chiricolo, Manfredi Tesauro and Giuseppe Massimo Sangiorgi

Biomedicines 2025, 13(6), 1470; https://doi.org/10.3390/biomedicines13061470 - 14 Jun 2025

Background/Objectives: Polymer-free drug-eluting stents (PF-DESs) aim to mitigate long-term adverse effects associated with polymer-based platforms. However, clinical comparisons with biodegradable polymer DESs (BP-DESs) remain limited. The objective of this review is to assess the efficacy and safety of PF-DESs versus thin-struts (<100 [...] Read more.

Background/Objectives: Polymer-free drug-eluting stents (PF-DESs) aim to mitigate long-term adverse effects associated with polymer-based platforms. However, clinical comparisons with biodegradable polymer DESs (BP-DESs) remain limited. The objective of this review is to assess the efficacy and safety of PF-DESs versus thin-struts (<100 μm) BP-DESs in patients undergoing percutaneous coronary intervention (PCI). Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing PF-DESs and BP-DESs in adults undergoing PCI. PubMed, Embase, and CENTRAL were searched up to 1 February 2025. A random-effects model was used to calculate pooled risk ratios (RR) or mean differences (MD) with 95% confidence intervals (CI). Outcomes included myocardial infarction (MI), all-cause and cardiac death, target lesion revascularization (TLR), stent thrombosis, and angiographic/OCT parameters. Subgroup and sensitivity analyses were conducted for outcomes with high heterogeneity (I² > 50%). Results: Nine RCTs (n = 9597) were included. At 12 months, no significant differences were found between PF-DESs and BP-DESs for TLR (RR 1.51; 95% CI: 0.83–2.75), MI, or stent thrombosis. At 24 months, MI and all-cause death were similar between groups. A subgroup analysis showed lower cardiac death with the BioFreedom stent (RR 0.57; 95% CI: 0.35–0.90), not observed in non-BioFreedom devices. No significant differences were detected in angiographic or OCT outcomes, though heterogeneity was high. Conclusions: PF-DESs and BP-DESs demonstrated comparable clinical performance. The observed benefit in cardiac death with BioFreedom may reflect device-specific effects and merits further investigation. Full article

(This article belongs to the Section Biomedical Engineering and Materials)

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16 pages, 1615 KiB

Open AccessArticle

A Word of Caution—Potential Limitations of Pulmonary Artery Pressure Monitoring in Detecting Congestion Caused by Right-Sided Heart Failure

by Ester Judith Herrmann, Eva Herrmann, Khodr Tello, Kathleen Mantzsch, Meaza Tekeste, Stephan Fichtlscherer, Christian W. Hamm and Birgit Assmus

Biomedicines 2025, 13(6), 1469; https://doi.org/10.3390/biomedicines13061469 - 14 Jun 2025

Background/Objectives: Patients with New York Heart Association (NYHA) class III heart failure (HF) suffer from frequent hospitalizations. Non-invasive pulmonary artery pressure (PAP) sensor-guided HF care has been shown to reduce hospitalizations. However, it is unknown whether the PAP changes prior to hospitalization differ [...] Read more.

Background/Objectives: Patients with New York Heart Association (NYHA) class III heart failure (HF) suffer from frequent hospitalizations. Non-invasive pulmonary artery pressure (PAP) sensor-guided HF care has been shown to reduce hospitalizations. However, it is unknown whether the PAP changes prior to hospitalization differ between clinical right, left or global cardiac decompensation. Methods: Sensor-derived PAP data and HF hospitalization records from 41 patients with NYHA class III HF were classified retrospectively into predominantly left, right or global decompensation. Linear mixed-effect regression models were used for statistical evaluations of the PAP in selected hospitalizations for which admission was at least 28 days after the last admission and 14 days after the last hospital discharge and with readings in between. Results: During 24.4 months of follow-up, 127 hospitalizations in 38 patients were evaluated. The global cardiac decompensation (n = 13) had the highest PAP before hospitalization, followed by left-sided (n = 20) decompensation. Patients with right-sided decompensation (n = 9) had comparable PAP values before hospitalization to the cohort without any cardiac decompensation (n = 85). The diastolic PAP showed a significant increase of 0.035 mmHg/day (p = 0.0097) in left-sided decompensation and of 0.13 mmHg/day (p < 0.0001) in global cardiac decompensation, whereas no significant change in the diastolic PAP occurred prior to the right-sided decompensation. The baseline right ventricular function and right ventricle–pulmonary arterial coupling (TAPSE/PASP ratio) were impaired in patients with subsequent global cardiac decompensation. Conclusion: PAP telemonitoring-guided therapy can reliably detect early signs of left and global cardiac decompensation but may be limited in detecting right-sided cardiac congestion. The routine assessment of RV–PA coupling may improve the detection of global cardiac decompensation, as severe impairments could indicate impending deterioration. In contrast, monitoring the RV contractility may aid in identifying isolated right-sided congestion and imminent decompensation. Full article

(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 2nd Edition)

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16 pages, 2192 KiB

Open AccessArticle

Proton Density of the Dorsal Root Ganglia in Classical Fabry Disease: MRI Correlates of Small Fibre Neuropathy

by Simon Weiner, Sarah Perleth, Charlotte Schäfer Gómez, Thomas Kampf, Kolja Lau, Florian Hessenauer, György Homola, Peter Nordbeck, Nurcan Üçeyler, Claudia Sommer, Mirko Pham and Magnus Schindehütte

Biomedicines 2025, 13(6), 1468; https://doi.org/10.3390/biomedicines13061468 - 13 Jun 2025

Background/Objectives: Fabry disease (FD) is a lysosomal storage disorder often associated with early-onset neuropathic pain, attributed to small fibre neuropathy (SFN). The dorsal root ganglion (DRG) has emerged as a critical site of early pathophysiological involvement in FD, with structural and functional alterations [...] Read more.

Background/Objectives: Fabry disease (FD) is a lysosomal storage disorder often associated with early-onset neuropathic pain, attributed to small fibre neuropathy (SFN). The dorsal root ganglion (DRG) has emerged as a critical site of early pathophysiological involvement in FD, with structural and functional alterations implicated in the development of neuropathic symptoms. This exploratory study introduces DRG proton density (DRG-PD) as a novel MRI-derived biomarker and evaluates its association with SFN. Methods: Eighty genetically confirmed FD patients underwent high-resolution 3T MRI with DRG-PD quantification at the lumbosacral levels L5 and S1. DRG-PD was derived from B1-corrected multi-echo spin echo sequences and normalised to cerebrospinal fluid intensity. All patients underwent clinical, biochemical and histological evaluation to determine SFN status. Associations between DRG imaging parameters and clinical variables were analysed using correlation and regression models. Diagnostic performance was evaluated using receiver operating characteristic curve analysis. Results: DRG-PD values were significantly increased in patients with classical FD and SFN, demonstrating a large effect size (Cliff’s δ = 0.92) and excellent discriminatory performance (AUC = 0.96). In contrast, DRG volume and T2 relaxation time were not significantly associated with SFN status. DRG-PD remained an independent predictor of SFN in multivariable logistic regression (p = 0.019). Conclusions: DRG-PD is a non-invasive correlate of SFN in classical FD. It may provide superior diagnostic value compared to existing MRI metrics and reflects proximal ganglionic pathology not captured by distal histological assessments. Full article

(This article belongs to the Special Issue Biomarkers in Pain)

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12 pages, 1727 KiB

Open AccessViewpoint

An Overview of Glutaminyl Cyclase as a Promising Drug Target for Alzheimer’s Disease

by Rasajna Madhusudhana, Emily Boyle and Yana Cen

Biomedicines 2025, 13(6), 1467; https://doi.org/10.3390/biomedicines13061467 - 13 Jun 2025

Alzheimer’s disease (AD) has become an increasingly pressing concern for the aging population. Current AD treatments mainly focus on cognitive and neuropsychiatric symptoms—with few FDA-approved treatments targeting disease progression itself. The amyloid cascade hypothesis describes the formation and accumulation of β-amyloid (Aβ) oligomers [...] Read more.

Alzheimer’s disease (AD) has become an increasingly pressing concern for the aging population. Current AD treatments mainly focus on cognitive and neuropsychiatric symptoms—with few FDA-approved treatments targeting disease progression itself. The amyloid cascade hypothesis describes the formation and accumulation of β-amyloid (Aβ) oligomers and plaques as a primary event in AD pathogenesis. This hypothesis has served as the foundation of disease-modifying treatment development over the last decade. Recently, glutaminyl cyclase (QC) has been identified as a potential drug target in the amyloid cascade. QC catalyzes the cyclization of Aβ to form pyroglutamated Aβ (pEAβ). pEAβ acts as the seed for the formation of Aβ plaques, thus preventing the formation of pEAβ via QC inhibition, and offers a promising therapeutic strategy against AD. Here, we offer an overview of the pathway QCI research has followed—from the initial testing of imidazole-based inhibitor scaffolds to QCI structural optimization via pharmacophore identification, Varoglutamstat entering clinical trials, and further avenues of bettering specificity and potency for future QCI development. Full article

(This article belongs to the Special Issue New Horizons in Enzyme Inhibitor Discovery: Targets, Design and Evaluation)

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19 pages, 1703 KiB

Open AccessArticle

Sex-Specific Impact of 17β-Estradiol and Testosterone Levels on Inflammation and Injury in Acute Myocardial Infarction—Preliminary Results

by Niya E. Semerdzhieva, Adelina D. Tsakova and Vesela V. Lozanova

Biomedicines 2025, 13(6), 1466; https://doi.org/10.3390/biomedicines13061466 - 13 Jun 2025

Background: Estrogens play a protective role during the early stages of life. However, endogenous 17β-estradiol (E2) can accelerate atherosclerosis progression. Aim: The purpose of this study was to test for the significance of the sex-specific associations of gonadal hormones with the extent of [...] Read more.

Background: Estrogens play a protective role during the early stages of life. However, endogenous 17β-estradiol (E2) can accelerate atherosclerosis progression. Aim: The purpose of this study was to test for the significance of the sex-specific associations of gonadal hormones with the extent of the inflammatory response, myocardial damage, and ventricular arrhythmia risk in acute myocardial infarction (MI). Materials and Methods: Study design: single-center cohort study. Blood samples for the assessment of sex steroids (E2, total testosterone [T]), oxidized low-density lipoproteins, high-sensitivity C-reactive protein (CRP), white blood cell (WBC) counts, and cardiac enzymes were collected 48 h after the onset of symptoms (and within 6 h after PCI) from 111 patients (37% women) with acute MI. Coronary disease severity, left ventricular systolic function (LV), and indices of ventricular repolarization were assessed using coronary angiography, echocardiography, and a conventional electrocardiogram, respectively. Results: In men with acute MI, peak cardiac enzyme levels were predicted by post-percutaneous coronary intervention (PCI) E2 plasma levels, peak WBC count, and peak CRP plasma levels. T levels and the E2/T ratio were associated with post-PCI CRP in these men. For women, peak WBC count was a marker of highest testosterone, and only WBC count was a significant indicator of myocardial injury extent. The incidence of acute ventricular tachycardia detected in AMI was significantly associated with left ventricular ejection fraction and with peak WBC count (as a tendency) regardless of sex. A longer duration of cardiac repolarization prior to PCI was predicted by lower ejection fractions in men and by age, CRP, and testosterone levels in female patients. Conclusions: During acute MI, elevated endogenous estradiol levels in men and increased leukocytes in women indicate acute myocardial damage. Post-PCI plasma inflammatory markers are sex-specific confounding factors for acute endogenous E2 levels, T levels, and the E2/T ratio. LV systolic function in men and, characteristically, the acute inflammatory response and testosterone levels in women are predictors of longer ventricular repolarization and arrhythmia risk. Full article

(This article belongs to the Special Issue Acute and Chronic Heart Failure: Pathophysiology and New Therapeutic Developments, 2nd Edition)

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18 pages, 785 KiB

Open AccessReview

Tubal Ectopic Pregnancy: From Diagnosis to Treatment

by Dimitrios Papageorgiou, Ioakeim Sapantzoglou, Ioannis Prokopakis and Eleftherios Zachariou

Biomedicines 2025, 13(6), 1465; https://doi.org/10.3390/biomedicines13061465 (registering DOI) - 13 Jun 2025

The most frequent form of ectopic pregnancy, known as tubal pregnancy, leads to a dangerous situation where the fertilized ovum implants inside a fallopian tube, which can result in tubal rupture and severe bleeding. The purpose of this narrative review is to evaluate [...] Read more.

The most frequent form of ectopic pregnancy, known as tubal pregnancy, leads to a dangerous situation where the fertilized ovum implants inside a fallopian tube, which can result in tubal rupture and severe bleeding. The purpose of this narrative review is to evaluate all existing data regarding epidemiology, risk factors, pathophysiology, clinical presentation, diagnosis, and management of tubal ectopic pregnancy in order to provide a comprehensive understanding of this common yet difficult clinical condition. Prior ectopic pregnancy, together with tubal pathology and assisted reproduction, represent the main risk factors for this condition. The diagnosis relies on serial β-hCG tests combined with transvaginal ultrasonography, but laparoscopy serves as the diagnostic tool for cases with uncertain results. The treatment plan depends on the fallopian tube integrity, along with the patient’s hemodynamic condition. Patients with unruptured pregnancies who are hemodynamically stable receive methotrexate treatment as the preferred option, but surgical intervention with salpingectomy or salpingostomy becomes necessary in case of tubal rupture or when medical treatment fails. The development of laparoscopic procedures has led to better results and improved possibilities for fertility preservation. The psychological effects on patients require both counseling and follow-up care. Early detection, along with personalized management, helps decrease maternal complications and optimize reproductive outcomes. Full article

(This article belongs to the Special Issue Maternal-Fetal and Neonatal Medicine)

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27 pages, 2139 KiB

Open AccessReview

Next-Generation Drug Delivery for Neurotherapeutics: The Promise of Stimuli-Triggered Nanocarriers

by Radka Boyuklieva, Nikolay Zahariev, Plamen Simeonov, Dimitar Penkov and Plamen Katsarov

Biomedicines 2025, 13(6), 1464; https://doi.org/10.3390/biomedicines13061464 - 13 Jun 2025

Nanotherapeutics have emerged as novel unparalleled drug delivery systems (DDSs) for the treatment of neurodegenerative disorders. By applying different technological approaches, nanoparticles can be engineered to possess different functionalities. In recent years, the developed, stimuli-responsive nanocarriers stand out as novel complex DDSs ensuring [...] Read more.

Nanotherapeutics have emerged as novel unparalleled drug delivery systems (DDSs) for the treatment of neurodegenerative disorders. By applying different technological approaches, nanoparticles can be engineered to possess different functionalities. In recent years, the developed, stimuli-responsive nanocarriers stand out as novel complex DDSs ensuring selective and specific drug delivery in response to different endogenous and exogenous stimuli. Due to the multifaceted pathophysiology of the nervous system, a major challenge in modern neuropharmacology is the development of effective therapies ensuring high efficacy and low toxicity. Functionalization of the nanocarriers to react to specific microenvironmental changes in the nervous system tissues or external stimulations significantly enhances the efficacy of drug delivery. This review discusses the microenvironmental characteristics of some common neurological diseases in-depth and provides a comprehensive overview on the progress of the development of exogenous and endogenous stimuli-sensitive nanocarriers for the treatment of Alzheimer’s and Parkinson’s disease. Full article

(This article belongs to the Special Issue Advanced Research in Neuroprotection)

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