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Mechanotransduction and Skeletal Muscle Atrophy: The Interplay Between Focal Adhesions and Oxidative Stress
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Epigenetic Echoes: Bridging Nature, Nurture, and Healing Across Generations
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TL1A as a Target in Inflammatory Bowel Disease: Exploring Mechanisms and Therapeutic Potential
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Nanozymes: Innovative Therapeutics in the Battle Against Neurodegenerative Diseases
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Breaking the Barrier: The Role of Proinflammatory Cytokines in BBB Dysfunction
Journal Description
International Journal of Molecular Sciences
International Journal of Molecular Sciences
is an international, peer-reviewed, open access journal providing an advanced forum for biochemistry, molecular and cell biology, molecular biophysics, molecular medicine, and all aspects of molecular research in chemistry, and is published semimonthly online by MDPI. The Australian Society of Plant Scientists (ASPS), Epigenetics Society, European Chitin Society (EUCHIS), Spanish Society for Cell Biology (SEBC) and others are affiliated with IJMS and their members receive a discount on the article processing charges.
- 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, MEDLINE, Embase, CAPlus / SciFinder, and other databases.
- Journal Rank: JCR - Q1 (Biochemistry and Molecular Biology) / CiteScore - Q1 (Organic Chemistry)
- Rapid Publication: manuscripts are peer-reviewed and a first decision is provided to authors approximately 20.5 days after submission; acceptance to publication is undertaken in 2.6 days (median values for papers published in this journal in the first half of 2025).
- 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.
- Testimonials: See what our editors and authors say about IJMS.
- Companion journals for IJMS include: Biophysica, Stresses, Lymphatics and SynBio.
Impact Factor:
4.9 (2024);
5-Year Impact Factor:
5.7 (2024)
Latest Articles
Seed-Specific Silencing of Abundantly Expressed Soybean Bowman–Birk Protease Inhibitor Genes by RNAi Lowers Trypsin and Chymotrypsin Inhibitor Activities and Enhances Protein Digestibility
Int. J. Mol. Sci. 2025, 26(14), 6943; https://doi.org/10.3390/ijms26146943 (registering DOI) - 19 Jul 2025
Abstract
Soybean meal (SBM) is extensively used as a predominant protein source in animal feed. However, raw soybean cannot be directly utilized in animal feed, due to the presence of the Kunitz trypsin inhibitor (KTi) and the Bowman–Birk protease inhibitor (BBi). These antinutritional factors
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Soybean meal (SBM) is extensively used as a predominant protein source in animal feed. However, raw soybean cannot be directly utilized in animal feed, due to the presence of the Kunitz trypsin inhibitor (KTi) and the Bowman–Birk protease inhibitor (BBi). These antinutritional factors inhibit the digestive enzymes in animals, trypsin and chymotrypsin, resulting in poor animal performance. To inactivate the activity of protease inhibitors, SBM is subjected to heat processing, a procedure that can negatively impact the soybean protein quality. Thus, it would be beneficial to develop soybean varieties with little or no trypsin inhibitors. In this study, we report on the creation of experimental soybean lines with significantly reduced levels of Bowman–Birk protease inhibitors. RNA interference (RNAi) technology was employed to generate several transgenic soybean lines. Some of these BBi knockdown soybean lines showed significantly lower amounts of both trypsin and chymotrypsin inhibitor activities. Western blot analysis revealed the complete absence of BBi in selected RNAi-derived lines. RNA sequencing (RNAseq) analysis demonstrated a drastic reduction in the seed-specific expression of BBi genes in the transgenic soybean lines during seed development. Confocal fluorescence immunolabeling studies showed that the accumulation of BBi was drastically diminished in BBi knockdown lines compared to wild-type soybeans. The absence of BBi in the transgenic soybean did not alter the overall protein, oil, and sulfur amino acid content of the seeds compared to wild-type soybeans. The seed protein from the BBi knockdown lines were more rapidly hydrolyzed by trypsin and chymotrypsin compared to the wild type, indicating that the absence of BBi enhances protein digestibility. Our study suggests that these BBi knockdown lines could be a valuable resource in order for plant breeders to incorporate this trait into commercial soybean cultivars, potentially enabling the use of raw soybeans in animal feed.
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(This article belongs to the Special Issue Genetics and Novel Techniques for Soybean Pivotal Characters)
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Wnt/β-Catenin Signaling Regulates Hepatitis B Virus cccDNA Levels
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Atsuya Ishida, Sadahiro Iwabuchi, Ying-Yi Li, Kazuhisa Murai, Takayoshi Shirasaki, Kazuyuki Kuroki, Tetsuro Shimakami, Koki Nio, Kazunori Kawaguchi, Tadashi Imafuku, Satoru Ito, Taro Yamashita, Shuichi Kaneko, Hiroshi Yanagawa, Kouji Matsushima, Masao Honda and Shinichi Hashimoto
Int. J. Mol. Sci. 2025, 26(14), 6942; https://doi.org/10.3390/ijms26146942 (registering DOI) - 19 Jul 2025
Abstract
Hepatitis B virus (HBV) specifically infects hepatocytes and has a complex life cycle owing to the stabilization and pooling of covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocytes. We previously reported that the suppression of dedicator of cytokinesis 11 (DOCK11)
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Hepatitis B virus (HBV) specifically infects hepatocytes and has a complex life cycle owing to the stabilization and pooling of covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocytes. We previously reported that the suppression of dedicator of cytokinesis 11 (DOCK11) decreases cccDNA and HBV-DNA levels and identified it as a new HBV therapeutic target. The DOCK11-associated gene, Wnt/β-catenin signaling regulator tankyrase (TNKS), was identified using in vitro methods; however, its function in the HBV life cycle remains unknown. Here, we used various inhibitors, antagonists, and short-hairpin RNA treatments related to TNKS signaling in HBV-infected hepatocytes. The role of TNKS-related Wnt/β-catenin signaling in the HBV life cycle was evaluated using immunoprecipitation assays with DOCK11 and bulk RNA sequencing methods. TNKS and Wnt/β-catenin signaling inhibitors significantly repressed cccDNA and HBV-DNA levels. Conversely, certain Wnt/β-catenin signaling agonists enhanced the HBV life cycle. DOCK11 directly binds to β-catenin to regulate HBV using its nuclear transport system. SKL2001, normally used as a Wnt/β-catenin signaling agonist, strongly reduced cccDNA in HBV-infected hepatocytes and in combination with entecavir predominantly eradicated HBV without cytotoxicity. Therefore, DOCK11 and other Wnt/β-catenin signaling molecules may be therapeutic targets to prevent persistent HBV infection.
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(This article belongs to the Section Molecular Biology)
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APOE Genotype-Stratified Meta-Analysis of Cognitive Decline Reveals Novel Loci for Language and Global Cognitive Function in Older Adults
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Vibha Acharya, Kang-Hsien Fan, Beth E. Snitz, Mary Ganguli, Steven T. DeKosky, Oscar L. Lopez, Eleanor Feingold and M. Ilyas Kamboh
Int. J. Mol. Sci. 2025, 26(14), 6940; https://doi.org/10.3390/ijms26146940 (registering DOI) - 19 Jul 2025
Abstract
Apolipoprotein E (APOE) allele 4 (APOE4), one of the robust genetic risk factors for AD, has also been associated with cognitive decline in terms of memory, executive function, language, and global cognitive function. APOE genotype-stratified analysis can help to
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Apolipoprotein E (APOE) allele 4 (APOE4), one of the robust genetic risk factors for AD, has also been associated with cognitive decline in terms of memory, executive function, language, and global cognitive function. APOE genotype-stratified analysis can help to identify additional genetic loci which might be masked due to a strong effect of APOE4. We conducted a genome-wide meta-analysis in APOE2 carriers, APOE4 carriers, and APOE 3/3 homozygote groups among 2969 non-Hispanic Whites aged ≥ 65 years using slopes of decline over time across five cognitive domains (attention, language, executive function, memory, and visuospatial function) and global cognitive function. We identified novel genome-wide significant associations for decline in global cognitive function in the intergenic region between RNU7-66P/RNA5SP208 at rs116379916 (p = 1.44 × 10−9) in the APOE 3/3 group and for decline in language in the intergenic region between LINC0221/DTWD2 at rs13187183 (p = 3.79 × 10−8) in APOE4 carriers. A previously reported locus for decline in attention near RASEF at rs6559700 (p = 9.95 × 10−9) was found to be confined to the APOE 3/3 group. We also found two sub-threshold significant associations in the APOE 2 group for decline in attention (IL1RL2/rs77127114; p = 8.64 × 10−8) and decline in language (YTHDC2/KCNN2, rs116191836; p = 5.66 × 10−8). Our study points to potential biological pathways pertaining to specific domains within each APOE genotype group, and the findings suggest that immune-related pathways, plasma levels of polysaturated fatty acids, and bitter taste receptors may play roles in cognitive decline. Our findings enhance the understanding of cognitive aging and provide a framework for future studies.
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(This article belongs to the Section Molecular Genetics and Genomics)
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Exploring the Impact of TP53 Mutation and Wild-Type Status on the Efficacy of Immunotherapy in Non-Small Cell Lung Cancer
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Alexander Yakobson, Ronen Brenner, Itamar Gothelf, Natalie Maimon Rabinovich, Ahron Yehonatan Cohen, Ashraf Abu Jama, Nashat Abu Yasin, Fahmi Abu Ghalion, Abed Agbarya and Walid Shalata
Int. J. Mol. Sci. 2025, 26(14), 6939; https://doi.org/10.3390/ijms26146939 (registering DOI) - 19 Jul 2025
Abstract
TP (tumor protein) 53 mutation status plays a critical role in cancer progression and may influence survival outcomes in non-small cell lung cancer (NSCLC) patients receiving immunotherapy. This study investigates the impact of TP53 mutation status and immunotherapy treatment on survival in NSCLC
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TP (tumor protein) 53 mutation status plays a critical role in cancer progression and may influence survival outcomes in non-small cell lung cancer (NSCLC) patients receiving immunotherapy. This study investigates the impact of TP53 mutation status and immunotherapy treatment on survival in NSCLC patients. This retrospective study analyzed NSCLC patients treated with pembrolizumab or ipilimumab plus nivolumab, stratified by TP53 mutation status and PD-L1 (programmed death-ligand 1) expression (<1%, 1–49%, >50%). Survival outcomes (overall survival (OS) and progression free survival (PFS) were assessed using Kaplan–Meier curves and log-rank tests, with subgroup analysis by histological subtype. In squamous cell cancer (SCC) patients, no significant differences in OS or PFS were found based on TP53 mutation status or treatment type. A trend toward improved survival was observed with pembrolizumab (p = 0.088). In adenocarcinoma patients, significant differences in OS and PFS were observed based on TP53 mutation status. Pembrolizumab showed superior survival outcomes compared to ipilimumab plus nivolumab in TP53 wild-type patients (p < 0.001). PD-L1 ≥ 1% also predicted better outcomes, especially in adenocarcinoma patients. TP53 mutation status and immunotherapy type significantly influence survival outcomes in NSCLC, particularly in adenocarcinoma patients. Pembrolizumab demonstrated superior efficacy in TP53 wild-type patients, with PD-L1 expression further refining survival predictions. These findings underscore the importance of personalized treatment strategies based on TP53 status and PD-L1 expression in NSCLC. Further studies are needed to validate these results and optimize treatment approaches.
Full article
(This article belongs to the Special Issue Transforming in Cancer Therapy: Advances in Immunotherapy and Tyrosine Kinase Inhibitors)
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Pyrroloquinoline Quinone (PQQ) Attenuates Hydrogen Peroxide-Induced Injury Through the Enhancement of Mitochondrial Function in Human Trabecular Meshwork Cells
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Sabrina Petricca, Antonio Matrone, Daria Capece, Irene Flati, Vincenzo Flati, Enrico Ricevuto, Giuseppe Celenza, Nicola Franceschini, Mirco Mastrangelo, Cristina Pellegrini, Loredana Cristiano, Giuseppe Familiari, Benedetta Cinque, Giovanna Di Emidio, Carla Tatone and Roberto Iorio
Int. J. Mol. Sci. 2025, 26(14), 6938; https://doi.org/10.3390/ijms26146938 (registering DOI) - 19 Jul 2025
Abstract
Mitochondrial metabolism in the trabecular meshwork (TM) plays a critical role in maintaining intraocular pressure homeostasis by supporting the energy-demanding processes involved in aqueous humour outflow. In primary open-angle glaucoma, oxidative stress impairs mitochondrial function, leading to TM dysfunction. Therefore, understanding and targeting
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Mitochondrial metabolism in the trabecular meshwork (TM) plays a critical role in maintaining intraocular pressure homeostasis by supporting the energy-demanding processes involved in aqueous humour outflow. In primary open-angle glaucoma, oxidative stress impairs mitochondrial function, leading to TM dysfunction. Therefore, understanding and targeting mitochondrial health in TM cells could offer a novel therapeutic strategy. Pyrroloquinoline quinone (PQQ) is a redox cofactor with antioxidant and mitochondrial-enhancing properties. However, its effects on human TM (HTM) cells remain largely unexplored. This study examined PQQ cytoprotective effects against H2O2-induced oxidative stress in HTM cells. Seahorse analyses revealed that PQQ alone improves mitochondrial respiration and ATP production. Moreover, PQQ mitigates H2O2-induced cellular damage and preserves mitochondrial function by normalising proton leak and increasing ATP levels. Furthermore, TEM and confocal microscopy showed that PQQ can partially alleviate structural damage, restoring mitochondrial network morphology, thereby leading to reduced cell death. Although these protective effects seem not to be mediated by changes in mitochondrial content or activation of the SIRT1/PGC1-α pathway, they may involve modulation of SIRT3, a key factor of mitochondrial metabolism and homeostasis. Overall, these results suggest that PQQ may represent a promising candidate for restoring mitochondrial function and reversing oxidative damage in HTM cells.
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(This article belongs to the Special Issue Mitochondrial Functions and Dynamics)
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Open AccessReview
SGLT2 Inhibitors: From Structure–Effect Relationship to Pharmacological Response
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Teodora Mateoc, Andrei-Luca Dumitrascu, Corina Flangea, Daniela Puscasiu, Tania Vlad, Roxana Popescu, Cristina Marina and Daliborca-Cristina Vlad
Int. J. Mol. Sci. 2025, 26(14), 6937; https://doi.org/10.3390/ijms26146937 (registering DOI) - 19 Jul 2025
Abstract
SGLT2 inhibitors have become increasingly used due to their effectiveness in improving not only type 2 diabetes but also cardiovascular, renal and hepatic diseases, as well as the obesity found in metabolic syndrome. Starting from the structure of gliflozins, modifications of the carbohydrate
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SGLT2 inhibitors have become increasingly used due to their effectiveness in improving not only type 2 diabetes but also cardiovascular, renal and hepatic diseases, as well as the obesity found in metabolic syndrome. Starting from the structure of gliflozins, modifications of the carbohydrate part, aglycone, and also the glycosidic bond between them can determine variations in pharmacokinetic and pharmacodynamic properties. SGLT2 inhibitors, in addition to reducing blood glucose levels, improve alterations in lipid metabolism by diverting excessively accumulated lipids in tissues towards mobilization, lipolysis, β-oxidation, ketogenesis and the utilization of ketone bodies. This enhances anti-inflammatory properties by decreasing the levels of some proinflammatory mediators and by modulating some cell signaling pathways. Thus, in this review, the intimate mechanisms by which SGLT2 inhibitors achieve these therapeutic effects in the various conditions belonging to metabolic syndrome and beyond were described, along with the structure–effect relationship with some specific features of each gliflozin. Starting from these findings, further modeling of these molecules may lead to the creation of new therapeutic uses. Further research is needed to broaden the range of indications and also eliminate adverse effects, such as phenomena leading to lower limb amputations.
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(This article belongs to the Special Issue New Insights into the Treatment of Metabolic Syndrome and Diabetes)
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Open AccessReview
The Role of Protein Kinases in the Suppressive Phenotype of Myeloid-Derived Suppressor Cells
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Aikyn Kali, Nurshat Abdolla, Yuliya V. Perfilyeva, Yekaterina O. Ostapchuk and Raikhan Tleulieva
Int. J. Mol. Sci. 2025, 26(14), 6936; https://doi.org/10.3390/ijms26146936 (registering DOI) - 19 Jul 2025
Abstract
Inflammation is a self-defense mechanism that controls the homeostasis of an organism, and its alteration by persistent noxious stimuli could lead to an imbalance in the regulation of inflammatory responses mediated by innate and adaptive immunity. During chronic inflammation, sustained exposure of myeloid
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Inflammation is a self-defense mechanism that controls the homeostasis of an organism, and its alteration by persistent noxious stimuli could lead to an imbalance in the regulation of inflammatory responses mediated by innate and adaptive immunity. During chronic inflammation, sustained exposure of myeloid cells to the various inflammatory signals derived from inflamed tissue could lead to the generation of myeloid cells with an immunosuppressive state, called myeloid-derived suppressor cells (MDSCs), which can exert protective or deleterious functions depending on the nature of signals and the specific inflammatory conditions created by different pathophysiological contexts. Initially identified in various tumor models and cancer patient samples, these cells have long been recognized as negative regulators of anti-tumor immunity. Consequently, researchers have focused on elucidating the molecular mechanisms underlying their potent immunosuppressive activity. As a key component of the signal transducing processes, protein kinases play a central role in regulating the signal transduction mechanisms of many cellular activities, including differentiation and immunosuppression. Over the past decade, at least a dozen kinases, including mechanistic target of rapamycin (mTOR), phosphoinositide 3-kinases (PI3Ks), TAM (Tyro3, Axl, Mer) family of receptor tyrosine kinases (TAM RTKs), mitogen-activated protein kinases (MAPKs), and others, have emerged as key contributors to the generation and differentiation of MDSCs. Here, we discuss the recent findings on these kinases that directly contribute to the immunosuppressive functions of MDSCs.
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(This article belongs to the Section Molecular Immunology)
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The Inositol-5-Phosphatase SHIP1: Expression, Regulation and Role in Acute Lymphoblastic Leukemia
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Patrick Ehm and Manfred Jücker
Int. J. Mol. Sci. 2025, 26(14), 6935; https://doi.org/10.3390/ijms26146935 (registering DOI) - 19 Jul 2025
Abstract
Despite the successes achieved in recent years in the treatment of childhood acute lymphoblastic leukemia (ALL), high-risk ALL in particular still represents a considerable challenge, with poorer outcomes. The PI3K/AKT/mTOR signaling pathway is frequently constitutively activated in ALL and consequently leads to unrestricted
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Despite the successes achieved in recent years in the treatment of childhood acute lymphoblastic leukemia (ALL), high-risk ALL in particular still represents a considerable challenge, with poorer outcomes. The PI3K/AKT/mTOR signaling pathway is frequently constitutively activated in ALL and consequently leads to unrestricted cell proliferation, without showing frequent mutations in the most important representatives of the signaling pathway. Recent studies have shown that fine balanced protein expression is a common way to adjust oncogenic B cell directed receptor signaling and to mediate malignant cell proliferation and survival in leukemic cells. Too low expression of inhibitory phosphatases can lead to constitutive signaling of kinases, which are important for cell proliferation and survival. In contrast, marked high expression levels of key phosphatases enable cells with distinct pronounced oncogenic B cell directed receptor signaling to escape negative selection by attenuating signal strength and thus raising the threshold for deletion checkpoint activation. One of the most important B cell receptor-dependent signaling cascades is the PI3K/AKT signaling pathway, with its important antagonist SHIP1. However, recent data show that the inositol-5-phosphatase SHIP1 is differentially expressed across the heterogeneity of the ALL subtypes, making the overall therapeutic strategy targeting SHIP1 more complex. The aim of this article is therefore to provide an overview of the current knowledge about SHIP1, its expression in the various subtypes of ALL, its regulation, and the molecules that influence its gene and protein expression, to better understand its role in the pathogenesis of leukemia and other human cancers.
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(This article belongs to the Collection Latest Review Papers in Molecular Oncology)
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Could Skin Autofluorescence Be a Useful Biomarker in Systemic Lupus Erythematosus? A Systematic Review
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Teodor Salmen, Claudia Cobilinschi, Andrei Mihăilescu, Bianca-Margareta Salmen, Gabriela-Claudia Potcovaru, Daniela Opris-Belinski, Narcis Copcă, Simona Caraiola, Florentina Negoi, Anca Pantea Stoian and Ioana Săulescu
Int. J. Mol. Sci. 2025, 26(14), 6934; https://doi.org/10.3390/ijms26146934 (registering DOI) - 19 Jul 2025
Abstract
Systemic lupus erythematosus (SLE) is a multifaceted autoimmune disease with a heterogeneous organ involvement, for which reliable biomarkers are still being studied. The implication of advanced glycation end products (AGEs), resulting from oxidative stress, and their interaction with the receptor for AGEs (RAGE)
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Systemic lupus erythematosus (SLE) is a multifaceted autoimmune disease with a heterogeneous organ involvement, for which reliable biomarkers are still being studied. The implication of advanced glycation end products (AGEs), resulting from oxidative stress, and their interaction with the receptor for AGEs (RAGE) has been studied in pathologies with chronic proinflammatory status, offering potential relevance in SLE. This systematic review aimed to evaluate the utility of skin autofluorescence (SAF)—a non-invasive proxy for AGE accumulation—as a biomarker for disease severity, activity, and impact in SLE patients. Following PRISMA guidelines, six studies assessing SAF and/or circulating AGEs and soluble RAGE (sRAGE) in SLE were analyzed. Findings consistently showed higher AGE levels in SLE patients compared to healthy controls, with several correlations between SAF/AGEs and disease features such as SLEDAI scores, organ involvement, inflammatory markers, and damage indices. Decreased sRAGE levels were also observed, possibly due to consumption by AGEs. Some studies further reported predictive associations between specific AGEs or their ratios with sRAGE and particular clinical phenotypes. Although heterogeneity among studies limits definitive conclusions, the AGEs–sRAGE axis—and especially SAF—emerges as a promising candidate for future biomarker development in SLE. Further large-scale longitudinal studies are needed to confirm its clinical utility.
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(This article belongs to the Special Issue Molecular Aspects of Autoimmune Diseases)
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Hemodialysis Intensifies NLRP3 Inflammasome Expression and Oxidative Stress in Patients with Chronic Kidney Disease
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Marcia Ribeiro, Ludmila F. M. F. Cardozo, Karen Salve Coutinho-Wolino, Marcelo Ribeiro-Alves and Denise Mafra
Int. J. Mol. Sci. 2025, 26(14), 6933; https://doi.org/10.3390/ijms26146933 (registering DOI) - 19 Jul 2025
Abstract
Chronic inflammation plays a central role in the progression and complications of chronic kidney disease (CKD). The nod-like receptor pyrin domain-containing 3 (NLRP3) inflammasome pathway has emerged as a crucial mediator of the inflammatory response in CKD. This cross-sectional study evaluated the expression
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Chronic inflammation plays a central role in the progression and complications of chronic kidney disease (CKD). The nod-like receptor pyrin domain-containing 3 (NLRP3) inflammasome pathway has emerged as a crucial mediator of the inflammatory response in CKD. This cross-sectional study evaluated the expression of NLRP3 in patients with CKD undergoing different treatments. Blood samples were collected from 32 non-dialysis (ND) patients [63 (11.2) years, estimated glomerular filtration rate, 43.5 (22.0) mL/min, BMI, 29.5 (10.0) kg/m2)], 50 hemodialysis (HD) patients [48.5 (16.5) years, 60.5 (50) months on HD, BMI, 24.2 (4.9) kg/m2)], and 8 peritoneal dialysis (PD) patients [56.5 (8.5) years, 40.5 (41.2) months on PD, BMI, 28.8 (2.6) kg/m2)]. The mRNA expression level of NLRP3 was measured using real-time PCR. The cytokines and the malondialdehyde (MDA) levels were also assessed. The results indicated that the mRNA level of NLRP3 was significantly elevated in patients undergoing HD (1.23, IQR = 0.95) compared with that in non-dialysis patients (0.79, IQR = 0.35) and in patients undergoing PD (0.77, IQR = 0.38) after adjusting for confounding variables, including age, sex, BMI, and dialysis duration. Furthermore, the MDA levels were significantly higher in HD patients. NLRP3 is upregulated in HD patients, and the results suggested that the inflammasome may be associated with oxidative stress in patients with CKD.
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(This article belongs to the Special Issue Nutrition, Inflammation, and Chronic Kidney Disease)
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Carbohydrate-Responsive Element-Binding Protein-Associated Metabolic Changes in Chemically Induced Hepatocarcinogenesis Mouse Model
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Maren Engeler, Majedul Karim, Marcel Gischke, Franziska Willer, Helen Leiner, Jessica Prey, Paul Friedrich Ziegler, Frank Dombrowski and Silvia Ribback
Int. J. Mol. Sci. 2025, 26(14), 6932; https://doi.org/10.3390/ijms26146932 - 18 Jul 2025
Abstract
The Carbohydrate-Responsive Element-Binding Protein (ChREBP) is a glucose-sensitive transcription factor that regulates the carbohydrate and lipid metabolism. We investigated its cell-type-specific role in hepatocarcinogenesis using a chemically induced mouse model. Additionally, we examined the functions of its isoforms, ChREBPα and ChREBPβ. After the
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The Carbohydrate-Responsive Element-Binding Protein (ChREBP) is a glucose-sensitive transcription factor that regulates the carbohydrate and lipid metabolism. We investigated its cell-type-specific role in hepatocarcinogenesis using a chemically induced mouse model. Additionally, we examined the functions of its isoforms, ChREBPα and ChREBPβ. After the diethylnitrosamine (DEN) administration, we analyzed hepatocellular adenomas and carcinomas in systemic ChREBP-knockout (KO), hepatocyte-specific ChREBP-KO (L-KO), and wildtype (WT) mice at 4, 12, and 36 weeks using histology, morphometry, proliferation measurements, immunohistochemistry, a Western blot, and a quantitative PCR. Tumors developed 36 weeks after the DEN administration in 27% of WT mice but less frequently in KO (18%) and L-KO (9%) mice. However, preneoplastic foci were less common in KO mice but not in L-KO mice (39% vs. 9%; p < 0.05). L-KO hepatocytes exhibited lower proliferation, while KO tumors showed the downregulation of AKT/mTOR signaling, glycolysis, and lipogenesis compared to WT tumors. Our results showed that the liver-specific loss of ChREBPα, while ChREBPβ remained active, significantly reduced the tumor progression, suggesting an oncogenic role for ChREBPα. In contrast, the systemic knockout of both ChREBPα and ChREBPβ reduced the tumor initiation but did slightly prevent tumor progression, indicating that ChREBPβ may exert tumor-suppressive functions.
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(This article belongs to the Special Issue Pathogenesis and Molecular Treatment of Primary Liver Cancer)
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NR4A1 Mediates Bronchopulmonary Dysplasia-Like Lung Injury Induced by Intrauterine Inflammation in Mouse Offspring
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Xiya Ding, Ruoxuan Li, Dongting Yao, Zhimin Lei, Wei Li, Qianwen Shen, Ze Chen, Meng Ni, Baihe Li, Xiaorui Liu, Jiuru Zhao, Qianqian Zhang and Zhiwei Liu
Int. J. Mol. Sci. 2025, 26(14), 6931; https://doi.org/10.3390/ijms26146931 - 18 Jul 2025
Abstract
Intrauterine inflammation (IUI) is involved in the development of bronchopulmonary dysplasia (BPD). Previously, we observed BPD-like pathological changes in a mouse model of IUI. This study aimed to identify the key molecules involved in IUI-induced lung injury, focusing on NR4A1. Pregnant C57BL/6 mice
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Intrauterine inflammation (IUI) is involved in the development of bronchopulmonary dysplasia (BPD). Previously, we observed BPD-like pathological changes in a mouse model of IUI. This study aimed to identify the key molecules involved in IUI-induced lung injury, focusing on NR4A1. Pregnant C57BL/6 mice were randomly divided into control and IUI groups. To verify the intervention effects, Nr4a1 siRNA was administered intranasally on postnatal day 3, while an NR4A1 overexpression plasmid was applied in MLE-12 cells to investigate downstream molecules. We found that the lungs of IUI-induced offspring exhibited a simplified structure on postnatal day 1 and excessive collagen fiber deposition by day 90. Postnatal NR4A1 intervention reversed IUI-induced neonatal lung injury. NR4A1 overexpression reduced cell proliferation and AKT and ERK1/2 phosphorylation levels, while also affecting the expression of the key epithelial–mesenchymal transition (EMT)-related gene TGF-β. EREG is a downstream target with potential NR4A1 binding sites in its promoter region. The expression of EMT-related genes can be recovered by blocking the receptor of EREG. Our findings imply that IUI induces BPD-like lung injury in neonates and fibrosis-like lung lesions in adult mice. The NR4A1-EREG-EGFR signaling pathway in pulmonary epithelial cells is crucial in IUI-induced lung injury, highlighting a key therapeutic target for mitigating BPD-like injury.
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(This article belongs to the Special Issue Molecular Mechanisms: New Insights into the Pathogenesis of Neonatal Disorders)
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A Quest for Effective 19F NMR Spectra Modeling: What Brings a Good Balance Between Accuracy and Computational Cost in Fluorine Chemical Shift Calculations?
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Stepan A. Ukhanev, Yuriy Yu. Rusakov and Irina L. Rusakova
Int. J. Mol. Sci. 2025, 26(14), 6930; https://doi.org/10.3390/ijms26146930 - 18 Jul 2025
Abstract
This work proposes a systematic study of different computational schemes for fluorine Nuclear Magnetic Resonance (19F NMR) chemical shifts, with special emphasis placed on the basis set issue. This study encompasses two stages of calculation, namely, the development of the computational
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This work proposes a systematic study of different computational schemes for fluorine Nuclear Magnetic Resonance (19F NMR) chemical shifts, with special emphasis placed on the basis set issue. This study encompasses two stages of calculation, namely, the development of the computational schemes for the geometry optimization of fluorine compounds and the NMR chemical shift calculations. In both stages, the performance of different density functional theory functionals is considered against the method of coupled-cluster singles and doubles (CCSD), with the latter representing a theoretical reference in this work. This exchange-correlation functional study is accompanied with a basis set study in both stages of calculation. Basis sets of different families, sizes, and valence-splitting levels are considered. Various locally dense basis sets (LDBSs) are proposed for the calculation of 19F NMR chemical shifts, and their performance is assessed by comparison of the calculated chemical shifts with both theoretical and experimental reference data. Overall, the pcS-3/pcS-2 LDBS scheme is recommended as the most balanced locally dense basis set scheme for fluorine chemical shift calculations.
Full article
(This article belongs to the Section Physical Chemistry and Chemical Physics)
Open AccessArticle
Genetic Landscape of Non-Remitting Neutropenia in Children and Chronic Idiopathic Neutropenia in Adults
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Alice Grossi, Grigorios Tsaknakis, Francesca Rosamilia, Marta Rusmini, Paolo Uva, Isabella Ceccherini, Maria Carla Giarratana, Diego Vozzi, Irene Mavroudi, Carlo Dufour, Helen A. Papadaki and Francesca Fioredda
Int. J. Mol. Sci. 2025, 26(14), 6929; https://doi.org/10.3390/ijms26146929 - 18 Jul 2025
Abstract
Non-remitting neutropenia in children and chronic idiopathic neutropenia (CIN) in adults have been described previously as peculiar subgroups of neutropenic patients carrying similar clinical and immunological features. The present collection comprising 25 subjects (16 adults and 9 children) mostly affected with mild (84%)
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Non-remitting neutropenia in children and chronic idiopathic neutropenia (CIN) in adults have been described previously as peculiar subgroups of neutropenic patients carrying similar clinical and immunological features. The present collection comprising 25 subjects (16 adults and 9 children) mostly affected with mild (84%) and moderate (16%) neutropenia aimed to identify the underlying (possibly common) genetic background. The phenotype of these patients resemble the one described previously: no severe infections, presence of rheumathological signs, leukopenia in almost all patients and lymphocytopenia in one-third of the cohort. The pediatric patients did not share common genes with the adults, based on the results of the multisample test, while some singular variants in neutropenia potentially associated with immune dysregulation likely consistent with the phenotype were found. SPINK5, RELA and CARD11 were retrieved and seem to be consistent with the clinical picture characterized by neutropenia associated to immune dysregulation. The enrichment and burden tests performed in comparison with a control group underline that the products of expression by the variants involved belong to the autoimmunity and immune regulation pathways (i.e., SPINK5, PTPN22 and PSMB9). Even with the limitation of this study’s low number of patients, these results may suggest that non-remitting neutropenia and CIN in adults deserve deep genetic study and enlarged consideration in comparison with classical neutropenia.
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(This article belongs to the Special Issue New Insights into Immune Dysregulation Disorders)
Open AccessArticle
Tumor-Associated Macrophages and Collagen Remodeling in Mammary Carcinomas: A Comparative Analysis in Dogs and Humans
by
Ana Paula Vargas Garcia, Marisa Salvi, Luana Aparecida Reis, Bárbara Regina Melo Ribeiro, Cristiana Buzelin Nunes, Ana Maria de Paula and Geovanni Dantas Cassali
Int. J. Mol. Sci. 2025, 26(14), 6928; https://doi.org/10.3390/ijms26146928 - 18 Jul 2025
Abstract
The tumor microenvironment (TME) plays a central role in cancer progression, with tumor-associated macrophages (TAMs) and extracellular matrix (ECM) components such as collagen being key modulators of invasiveness and immune regulation. Although macrophage infiltration and ECM remodeling are well-documented individually, their coordinated contribution
[...] Read more.
The tumor microenvironment (TME) plays a central role in cancer progression, with tumor-associated macrophages (TAMs) and extracellular matrix (ECM) components such as collagen being key modulators of invasiveness and immune regulation. Although macrophage infiltration and ECM remodeling are well-documented individually, their coordinated contribution to mammary carcinoma aggressiveness remains underexplored, particularly in comparative oncology models. This study analyzed 117 mammary carcinoma samples—59 from dogs and 58 from women—using immunohistochemistry, immunofluorescence, and second-harmonic-generation (SHG) microscopy. We quantified TAM density and phenotype (CD206, iNOS, and S100A8/A9), assessed collagen fiber organization, and examined correlations with clinical–pathological variables and overall survival. Increased TAM infiltration was associated with a higher histological grade, aggressive molecular subtypes, enhanced cell proliferation, and shortened survival in dogs. High TAM density also correlated with decreased collagen fiber length and increased alignment, suggesting active immune–matrix remodeling in aggressive tumors. Macrophage phenotyping revealed heterogeneous populations, with CD206+ cells predominating in high-grade tumors, while S100A8/A9+/iNOS+ phenotypes were enriched in less aggressive subtypes. The findings were consistent across species, reinforcing the relevance of canine models. Our results identify macrophage–collagen interactions as critical determinants of tumor aggressiveness in mammary carcinomas. This study bridges comparative oncology and translational research by proposing immune–ECM signatures as potential prognostic biomarkers and therapeutic targets. These insights contribute to the advancement of molecular oncology in Brazil by supporting innovative strategies that integrate immune modulation and matrix-targeted interventions in breast cancer.
Full article
(This article belongs to the Special Issue State-of-the-Art Molecular Oncology in Brazil, 3rd Edition)
Open AccessArticle
Inhibitory Effects of Vandetanib on Catecholamine Synthesis in Rat Pheochromocytoma PC12 Cells
by
Yoshihiko Itoh, Kenichi Inagaki, Tomohiro Terasaka, Eisaku Morimoto, Takahiro Ishii, Kimitomo Yamaoka, Satoshi Fujisawa and Jun Wada
Int. J. Mol. Sci. 2025, 26(14), 6927; https://doi.org/10.3390/ijms26146927 - 18 Jul 2025
Abstract
Gain-of-function gene alterations in rearranged during transfection (RET), a receptor tyrosine kinase, are observed in both sporadic and hereditary medullary thyroid cancers (MTCs) and pheochromocytomas and paragangliomas (PPGLs). Several tyrosine kinase inhibitors (TKIs) that target RET have been proven to be effective on
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Gain-of-function gene alterations in rearranged during transfection (RET), a receptor tyrosine kinase, are observed in both sporadic and hereditary medullary thyroid cancers (MTCs) and pheochromocytomas and paragangliomas (PPGLs). Several tyrosine kinase inhibitors (TKIs) that target RET have been proven to be effective on MTCs and PCCs. Recently, TKIs, namely, sunitinib and selpercatinib, which were clinically used to target PPGLs, have been reported to decrease catecholamine levels without reducing tumor size. Our clinical case of metastatic medullary thyroid cancer, which is associated with RET mutations undergoing treatment with vandetanib, also suggests that vandetanib can decrease catecholamine levels. Therefore, we investigated the effect of vandetanib, a representative multi-targeted TKI for RET-related MTC, on cell proliferation and catecholamine synthesis in rat pheochromocytoma PC12 cells. Vandetanib reduced viable cells in a concentration-dependent manner. The dopamine and noradrenaline levels of the cell lysate were reduced in a concentration-dependent manner. They also decreased more prominently at lower concentrations of vandetanib compared to the inhibition of cell proliferation. The RNA knockdown study of Ret revealed that this inhibitory effect on catecholamine synthesis is mainly mediated by the suppression of RET signaling. Next, we focused on two signaling pathways downstream of RET, namely, ERK and AKT signaling. Treatment with vandetanib reduced both ERK and AKT phosphorylation in PC12 cells. Moreover, both an MEK inhibitor U0126 and a PI3K/AKT inhibitor LY294002 suppressed catecholamine synthesis without decreasing viable cells. This study in rat pheochromocytoma PC12 cells reveals the direct inhibitory effects of vandetanib on catecholamine synthesis via the suppression of RET-ERK and RET-AKT signaling.
Full article
(This article belongs to the Section Molecular Endocrinology and Metabolism)
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Open AccessArticle
Association of Cord Blood Metabolic Biomarkers (Leptin, Adiponectin, IGF-1) with Fetal Adiposity Across Gestation
by
Junko Tamai, Satoru Ikenoue, Keisuke Akita, Keita Hasegawa, Toshimitsu Otani, Marie Fukutake, Yoshifumi Kasuga and Mamoru Tanaka
Int. J. Mol. Sci. 2025, 26(14), 6926; https://doi.org/10.3390/ijms26146926 - 18 Jul 2025
Abstract
Childhood obesity is a substantial health problem worldwide. The origin of obesity (increased adiposity) can be partly traced back to intrauterine life. However, the determinants of fetal fat deposition remain unclear. This study investigated the association between cord blood adipocytokines related to lipid
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Childhood obesity is a substantial health problem worldwide. The origin of obesity (increased adiposity) can be partly traced back to intrauterine life. However, the determinants of fetal fat deposition remain unclear. This study investigated the association between cord blood adipocytokines related to lipid metabolism (leptin, adiponectin, and insulin-like growth factor-1 [IGF-1]) and fetal adiposity during gestation. A prospective study was conducted in a cohort of 94 singleton pregnancies. Fetal ultrasonography was performed at 24, 30, and 36 weeks of gestation. Estimated fetal adiposity (EFA) was calculated by integrating measurements of cross-sectional arm and thigh fat area percentages and anterior abdominal wall thickness. Plasma cytokine levels and C-peptide immunoreactivity (as a proxy for fetal insulin resistance) were evaluated in cord blood samples obtained at delivery. The associations of cord blood leptin, adiponectin and IGF-1 levels with EFA at 24, 30, and 36 weeks were determined by multiple linear regression, adjusted for potential covariates. The multivariate analyses indicated that leptin was significantly correlated with EFA at 30 and 36 weeks. Leptin was also positively correlated with C-peptide immunoreactivity in the umbilical cord. Cord adiponectin levels were not associated with EFA across gestation. Cord IGF-1 levels were significantly correlated with EFA and estimated fetal body weight (EFW) at 36 weeks. In conclusion, cord leptin was associated with EFA at 30 and 36 weeks, and IGF-1 was associated with EFA at 36 and EFW at 36 weeks. In Conclusion, cord leptin was associated with EFA at 30 and 36 weeks, and IGF-1 was associated with EFA and EFW at 36 weeks. Considering the effects of leptin and IGF-1 on fetal insulin resistance and lipid metabolism, increased levels of leptin and IGF-1 are potential plasma biomarkers of increased fetal adiposity, which may predispose to infant obesity and metabolic dysfunction in later life.
Full article
(This article belongs to the Special Issue Obesity: From Molecular Mechanisms to Clinical Aspects)
Open AccessReview
Integrating Redox Proteomics and Computational Modeling to Decipher Thiol-Based Oxidative Post-Translational Modifications (oxiPTMs) in Plant Stress Physiology
by
Cengiz Kaya and Francisco J. Corpas
Int. J. Mol. Sci. 2025, 26(14), 6925; https://doi.org/10.3390/ijms26146925 - 18 Jul 2025
Abstract
Redox signaling is central to plant adaptation, influencing metabolic regulation, stress responses, and developmental processes through thiol-based oxidative post-translational modifications (oxiPTMs) of redox-sensitive proteins. These modifications, particularly those involving cysteine (Cys) residues, act as molecular switches that alter protein function, structure, and interactions.
[...] Read more.
Redox signaling is central to plant adaptation, influencing metabolic regulation, stress responses, and developmental processes through thiol-based oxidative post-translational modifications (oxiPTMs) of redox-sensitive proteins. These modifications, particularly those involving cysteine (Cys) residues, act as molecular switches that alter protein function, structure, and interactions. Advances in mass spectrometry-based redox proteomics have greatly enhanced the identification and quantification of oxiPTMs, enabling a more refined understanding of redox dynamics in plant cells. In parallel, the emergence of computational modeling, artificial intelligence (AI), and machine learning (ML) has revolutionized the ability to predict redox-sensitive residues and characterize redox-dependent signaling networks. This review provides a comprehensive synthesis of methodological advancements in redox proteomics, including enrichment strategies, quantification techniques, and real-time redox sensing technologies. It also explores the integration of computational tools for predicting S-nitrosation, sulfenylation, S-glutathionylation, persulfidation, and disulfide bond formation, highlighting key models such as CysQuant, BiGRUD-SA, DLF-Sul, and Plant PTM Viewer. Furthermore, the functional significance of redox modifications is examined in plant development, seed germination, fruit ripening, and pathogen responses. By bridging experimental proteomics with AI-driven prediction platforms, this review underscores the future potential of integrated redox systems biology and emphasizes the importance of validating computational predictions, through experimental proteomics, for enhancing crop resilience, metabolic efficiency, and precision agriculture under climate variability.
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(This article belongs to the Section Molecular Plant Sciences)
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Open AccessReview
Rethinking Osteoporosis Drugs: Can We Simultaneously Address Sarcopenia?
by
Zoran Gavrilov and Jasna Lojk
Int. J. Mol. Sci. 2025, 26(14), 6924; https://doi.org/10.3390/ijms26146924 - 18 Jul 2025
Abstract
Osteoporosis and sarcopenia are two aspects of the geriatric syndrome that frequently occur together and affect one another in a condition referred to as osteosarcopenia. Preventive and treatment options for osteosarcopenia exist but are mainly focused on the treatment of osteoporosis, as there
[...] Read more.
Osteoporosis and sarcopenia are two aspects of the geriatric syndrome that frequently occur together and affect one another in a condition referred to as osteosarcopenia. Preventive and treatment options for osteosarcopenia exist but are mainly focused on the treatment of osteoporosis, as there is still no FDA-approved treatment for sarcopenia. Drugs for osteoporosis include antiresorptive and anabolic drugs and hormonal replacement therapies and are prescribed based on age, BMD and other patient characteristics, which, however, do not include the possible co-existence of sarcopenia. As several studies and clinical trials have shown that the pharmacological treatment of osteoporosis can also affect muscle tissue, in either a positive or negative manner, sarcopenia should be another factor affecting the choice of treatment, especially when facing equal treatment options for osteoporosis. The aim of this review was to summarize our current knowledge on the effects of FDA-approved drugs for the treatment of osteoporosis on muscle quality, mass and function. A better understanding of the effects that certain drugs have on muscle tissue might in the future help us to simultaneously at least partially also address the wasting of muscle tissue and avoid further pharmacologically induced decline.
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(This article belongs to the Section Molecular Pharmacology)
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Open AccessArticle
Abscisic Acid Enhances Ex Vitro Acclimatization Performance in Hop (Humulus lupulus L.)
by
Luciana Di Sario, David Navarro-Payá, María F. Zubillaga, José Tomás Matus, Patricia A. Boeri and Gastón A. Pizzio
Int. J. Mol. Sci. 2025, 26(14), 6923; https://doi.org/10.3390/ijms26146923 - 18 Jul 2025
Abstract
Humulus lupulus L. (hop) is a multipurpose crop valued for its essential role in beer production and for its bioactive compounds with recognized medicinal properties. Otherwise, climate change represents a major challenge to agriculture, particularly impacting the cultivation of crops with stenoecious characteristics,
[...] Read more.
Humulus lupulus L. (hop) is a multipurpose crop valued for its essential role in beer production and for its bioactive compounds with recognized medicinal properties. Otherwise, climate change represents a major challenge to agriculture, particularly impacting the cultivation of crops with stenoecious characteristics, such as hop. This highlights the urgent need to enhance crop resilience to adverse environmental conditions. The phytohormone abscisic acid (ABA) is a key regulator of plant responses to abiotic stress, yet the ABA signaling pathway remains poorly characterized in hop. Harnessing the publicly available hop genomics resources, we identified eight members of the PYRABACTIN RESISTANCE 1 LIKE ABA receptor family (HlPYLs). Phylogenetic and gene structure analyses classified these HlPYLs into the three canonical ABA receptor subfamilies. Furthermore, all eight HlPYLs are likely functional, as suggested by the protein sequence visual analysis. Expression profiling indicates that ABA perception in hop is primarily mediated by the HlPYL1-like and HlPYL8-like subfamilies, while the HlPYL4-like group appears to play a more limited role. Structure modeling and topology predictions of HlPYL1b and HlPYL2 provided insights into their potential functional mechanisms. To assess the physiological relevance of ABA signaling in hop, we evaluated the impact of exogenous ABA application during the ex vitro acclimatization phase. ABA-treated plants exhibited more robust growth, reduced stress symptoms, and improved acclimatization success. These effects were associated with reduced leaf transpiration and enhanced stomatal closure, consistent with ABA-mediated drought tolerance mechanisms. Altogether, this study provides the first comprehensive characterization of ABA receptor components in hop and demonstrates the practical utility of ABA in improving plant performance under ex vitro conditions. These findings lay the groundwork for further functional studies and highlight ABA signaling as a promising target for enhancing stress resilience in hop, with broader implications for sustainable agriculture in the face of climate change.
Full article
(This article belongs to the Special Issue The Role of Phytohormones in Plant Biotic/Abiotic Stress Tolerance)

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