Current molecular medicine最新文献

{"title":"SCH79797, an Antiplatelet Agent, Alleviates Restenosis by Inducing Apoptosis via p53-Mediated Mitochondrial Depolarization and Inhibiting Thrombus Formation after Angioplasty.","authors":"Ting-Lin Yen, Kun-Jing Hong, Jing-Shiun Jan, Yi-Ling Chen, Po-Ching Chou, Chieh-Yu Chen, Wen-Chin Ko","doi":"10.2174/0115665240375398250916093346","DOIUrl":"https://doi.org/10.2174/0115665240375398250916093346","url":null,"abstract":"<p><strong>Introduction: </strong>In the field of interventional cardiology, coronary in-stent restenosis (ISR) continues to present a clinical hurdle, even with the progress made in stent design and pharmacological interventions. While drug-eluting stents (DESs) and drug-eluting balloons (DEBs) have markedly decreased the occurrence of ISR when compared to bare-metal stents, the condition persists as a complication in revascularization, contributing to increased patient morbidity and challenging long-term treatment outcomes. Thus, a deeper understanding of ISR mechanisms and the development of novel therapeutic approaches are crucial for improving patient outcomes.</p><p><strong>Methods: </strong>In this study, we utilized the A10 cell as an in vitro model and induced common carotid artery balloon dilation injury in Sprague-Dawley rats as an animal model to explore the potential clinical applications of SCH79797, particularly in the treatment of ISR.</p><p><strong>Results: </strong>SCH79797, a protease-activated receptor-1 antagonist, induced apoptosis of smooth muscle cells through various pathways. SCH79797 promoted apoptosis via JNK/c-Jun and p53 upregulation in the cytosol. We also observed an increased Bax/Bcl-2 ratio in mitochondria, p53 translocation to mitochondria, and changes in the mitochondrial membrane potential to mitochondrial membrane permeabilization. Our comparative analysis with vorapaxar revealed the apoptotic effects of SCH79797 to be independent of its PAR-1 antagonist activity. Furthermore, SCH79797 administration significantly reduced common carotid artery restenosis and thrombosis following balloon injury in vivo.</p><p><strong>Discussion: </strong>Our study has been the first to demonstrate SCH79797 to directly induce VSMC apoptosis via the p53-mediated mitochondrial pathway, providing a novel mechanistic insight into ISR treatment. Unlike traditional anti-proliferative agents used in DESs, SCH79797 uniquely combines apoptotic induction with antithrombotic effects, making it a dual-action therapeutic candidate. This research study has laid the groundwork for localized drug-eluting strategies that can leverage SCH79797's properties to prevent ISR more effectively while minimizing systemic side effects.</p><p><strong>Conclusion: </strong>Our findings have established SCH79797 as a promising candidate for reducing ISR through apoptosis modulation. By leveraging the p53-mediated mitochondrial apoptotic pathway, SCH79797 may provide a groundbreaking approach to reducing restenosis. These findings could offer significant implications for the future development of targeted drug-eluting strategies by locally delivering SCH79797 in a controlled manner using DES or DEB, presenting SCH79797 as a transformative candidate in interventional cardiology.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ELOVL4 is a Prognostic Biomarker with Implications for Immune Modulation and Therapeutic Response in Gastric Cancer.","authors":"Yuxin Chu, Yi Yao, Qibin Song","doi":"10.2174/0115665240356824250116103049","DOIUrl":"https://doi.org/10.2174/0115665240356824250116103049","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) remains a major health burden with poor prognosis, highlighting the need for reliable prognostic biomarkers and therapeutic targets. ELOVL4 (Elongation of Very Long Chain Fatty Acids Protein 4) is an enzyme involved in lipid metabolism, which has been implicated in various cancers, but its role in GC remains largely unexplored.</p><p><strong>Methods: </strong>We evaluated the prognostic value of ELOVL4 expression in GC based on samples from The Cancer Genome Atlas (TCGA) database. Subsequently, we investigated the associations between ELOVL4 expression and tumor immune microenvironment features, including tumor microenvironment (TME) scores, immune cell infiltration, and immune checkpoint gene expression. Moreover, we assessed the correlation between ELOVL4 expression and tumor mutational burden (TMB) as well as drug sensitivity profiles. Functional and pathway enrichment analyses were performed to gain mechanistic insights.</p><p><strong>Results: </strong>High ELOVL4 expression was significantly associated with adverse clinical outcomes. A nomogram incorporating ELOVL4 expression was developed for individualized prognosis evaluation. Patients with high ELOVL4 expression exhibited an activated TME, with distinct immune cell infiltration patterns and correlations with immune checkpoint gene expression. Additionally, ELOVL4 expression was negatively correlated with TMB. Differential drug sensitivity profiles were identified between the high and low ELOVL4 expression groups. Enrichment analyses revealed the involvement of ELOVL4 in various biological processes and signaling pathways.</p><p><strong>Conclusion: </strong>Our findings establish ELOVL4 as a biomarker for poor prognosis and therapeutic target in GC, with implications for prognosis evaluation, immune microenvironment modulation, and chemotherapeutic response.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astragalus Mongholicus for Idiopathic Pulmonary Fibrosis Treatment: From Molecules to Systems.","authors":"Yimin Yang, Jianxing Guo, Guowei Ye, Nan Li","doi":"10.2174/0115665240396394250911235834","DOIUrl":"https://doi.org/10.2174/0115665240396394250911235834","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease with limited treatment options. Astragalus mongholicus (AM), a cornerstone herb in traditional Chinese medicine (TCM), demonstrates significant therapeutic potential for IPF due to its multi-target mechanisms. This review synthesizes evidence on AM and its bioactive components; astragalus polysaccharide (APS), astragaloside IV (AS IV), and calycosin (CAL) in targeting key IPF pathological processes. These include suppression of inflammatory responses (via TLR4/NF-κB inhibition), inhibition of extracellular matrix deposition (via MMP/TIMP modulation), attenuation of oxidative stress, regulation of autophagy, and blockade of epithelial-mesenchymal transition (via lncRNA-ATB/miR-200c/ZEB1 axis). We further highlight the integration of molecularlevel mechanisms with systems pharmacology to elucidate AM's holistic actions. Clinical studies support AM-containing TCM prescriptions in improving lung function with fewer adverse effects. This synthesis underscores AM's promise as a multi-target therapeutic agent and advocates for systematic pharmacology approaches in future IPF drug development.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Epigenetic Landscape of Hemophilia.","authors":"Swaroop Kumar Pandey, Ayush Kulshreshtha, Anuja Mishra","doi":"10.2174/0115665240400998250909063344","DOIUrl":"https://doi.org/10.2174/0115665240400998250909063344","url":null,"abstract":"<p><p>Hemophilia, a rare inherited bleeding illness that needs to be managed throughout one's life to stop bleeding episodes and lessen complications. Although the genetic foundation of hemophilia is well documented, recent research has demonstrated that epigenetic pathways can influence the severity of the disease, the effectiveness of treatment, and the occurrence of complications. Advances in epigenetic research have made it possible to better understand the complexities of hemophilia and design suitable and targeted treatments. Emerging advancements as well as challenges are explored within many countries around the globe. Several epigenetic factors influence how the disorder manifests and its severity. Therapeutic interventions are the cornerstone for treating the disorder. The epigenetic regulation of the principal hemophilia genes (F8/F9) is still not fully understood. With the right treatment, preventative strategies, and better healthcare protocols, hemophilia cases in a confined area can be decreased. We explore the intricate blood clotting processes, inheritance patterns, and genetic changes that contribute to hemophilia's pathophysiology. The current understanding of epigenetics in hemophilia is examined in this review, with particular attention paid to non-coding RNAs, histone changes, and DNA methylation.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Rho-Associated Kinase in the Cognitive Benefits of the ACE Inhibitory Peptide LAP for Hypertension.","authors":"Junling Huang, Haifeng Wang, Yang Liu, Bangzhen Luo, Hong Fang, Ming Luo","doi":"10.2174/0115665240408227250917073210","DOIUrl":"https://doi.org/10.2174/0115665240408227250917073210","url":null,"abstract":"<p><strong>Introduction: </strong>This study assessed the effects of the synthesized ACE inhibitory peptide LAP (Leu-Arg-Pro-Val-Ala-Ala) on cognitive impairment in hypertensive rats.</p><p><strong>Methods: </strong>Rho-associated coiled-coil containing protein kinase (ROCK) activity in peripheral blood mononuclear cells (PBMCs) was initially measured in elderly patients with hypertension and cognitive impairment using western blot analysis. The effect of LAP on the ROCK pathway was studied in a human cell line with ROCK1. Fifteenweek- old male spontaneously hypertensive rats (SHR) received intragastric LAP (500 μg/week) for eight weeks. Cognitive function was assessed using the Morris water maze test, and thoracic aorta remodeling was evaluated by determining the media/lumen ratio through immunohistochemistry. Amyloid beta (Aβ), phosphorylated tau (p-tau), and apoptotic neurons in the hippocampus were examined by western blot analysis and immunohistochemistry. Protein expression and activation related to the ROCK pathway, including moesin, myosin light chain (MLC), and myosin phosphatase target subunit (MYPT), were analyzed in the aorta and hippocampus using western blot and immunohistochemistry.</p><p><strong>Results: </strong>Hypertensive patients with cognitive impairment showed increased phosphorylated/total myosin-binding subunit ratios in PBMCs, indicating higher ROCK pathway activity. In vitro, LAP reduced p-moesin levels, confirming ROCK inhibition. In vivo, oral LAP lowered blood pressure and heart rate in SHR models and improved cognitive function. LAP also reduced aortic remodeling, decreased hippocampal Aβ and p-tau deposition, reduced neuronal apoptosis, and increased neuronal survival. Mechanistically, LAP inhibited ROCK pathway activation in the aorta and hippocampus, similar to the ROCK inhibitor fasudil.</p><p><strong>Discussion: </strong>Hypertension contributes to neurodegenerative changes through the activation of the ROCK signaling pathway. The study found that the ACE inhibitory peptide LAP not only sustainably lowered blood pressure, but also inhibited the ROCK pathway, reducing hippocampal Aβ and p-tau deposition, thereby offering a dual therapeutic approach for hypertension-related cognitive impairment.</p><p><strong>Conclusion: </strong>LAP alleviated hypertension-related cognitive impairment in SHR by inhibiting the hippocampal ROCK pathway, showing therapeutic potential.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Sema3F on VEGF in Primary Rat Hippocampal Neurons In vitro.","authors":"Cai-Xia Li, E Rihemuqiqige, Ting Lv, Jun-Xian Fu, Xiao-Yang Liu, Rong Tang, Guang-Lu Yang","doi":"10.2174/0115665240393105250910123016","DOIUrl":"https://doi.org/10.2174/0115665240393105250910123016","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to explore the mechanism of semaphorin 3F- (Sema3F) induced hippocampal axonal growth cone collapse by studying the effect of Sema3F on vascular endothelial growth factor (VEGF) in vitro primary rat hippocampal neuron culture system.</p><p><strong>Methods: </strong>Hippocampal neurons were taken from Wistar rats within 24 hours after birth for primary culture in vitro. On the third day, Sema3F was added to the experimental group, and fetal bovine serum at the same concentration was added to the control group. The cells were collected at 0, 5, 15, and 30 min. The expression of VEGF messenger ribonucleic acid (mRNA) in the hippocampal neurons was detected by real-time polymerase chain reaction (PCR), while VEGF expression was detected by Western blot. The level of VEGF expression in the hippocampal neuron culture medium was detected by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>The expression of both VEGF mRNA and VEGF protein in the rats' hippocampal neurons decreased at different times. The VEGF concentration in the culture medium initially increased before decreasing over time.</p><p><strong>Discussion: </strong>Sema3F is known to induce growth cone collapse in hippocampal neurons, and this study provides evidence that this effect may be mediated by downregulating VEGF expression and secretion. The initial increase in VEGF concentration in the culture medium could be a compensatory response to the collapse of growth cones, while the subsequent decrease suggests a sustained effect of Sema3F on VEGF regulation. The findings highlight the complex interplay between Sema3F and VEGF in neuronal development and repair. Future research should explore the underlying signaling pathways and potential therapeutic applications of these interactions.</p><p><strong>Conclusion: </strong>Sema3F inhibited the synthesis of VEGF in hippocampal neurons at transcription and translation levels in a time-dependent manner. Sema3F may also affect the secretion level of VEGF, initially increasing its extracellular expression before decreasing it over time.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamin-Related Protein 1 and the NLRP3 Inflammasome in Parkinson's Disease: Mechanistic Insights and Therapeutic Opportunities.","authors":"Chethan Konasuru Someshwar, Kamsagara Linganna Krishna","doi":"10.2174/0115665240397746250915001750","DOIUrl":"https://doi.org/10.2174/0115665240397746250915001750","url":null,"abstract":"<p><strong>Introduction: </strong>Parkinson's disease (PD) is characterized by the progressive destruction of the dopaminergic cells in the substantia nigra region. The incidence of PD continues to rise, with over 8.5 million people affected in 2019 and projections indicating it could reach over 17 million by 2040 compared with levels observed since 1980. This review examines the mechanistic role of Dynamin-Related Protein 1 (Drp1) and Nod-Like Receptor Family Pyrin Domain-Containing 3 (NLRP3) inflammasome in the development and pathogenesis of PD.</p><p><strong>Methods: </strong>The information was collected from databases such as PubMed, Embase, Google Scholar, Web of Science, and Elsevier database.</p><p><strong>Results: </strong>There is a potential for Drp1 and NLRP3 pathways to serve as therapeutic targets in PD. Drp1 inhibitors, such as Mdivi-1, aid in mediating mitochondrial homeostasis, and NLRP3 inhibitors prevent inflammation. Natural compounds that modulate such pathways include resveratrol and curcumin, and preclinical models demonstrate multi-target neuroprotection via direct antioxidant and anti-inflammatory properties.</p><p><strong>Discussion: </strong>The intricate relationship among oxidative stress, mitochondrial dynamics and inflammation indicates that a combination drug therapy approach is more likely to be effective compared to a single-agent strategy. In a subsequent phase, there is a need for improved formulation and enhancement of natural compounds to maximize their bioavailability and efficacy, particularly in terms of selective Drp1 and NLRP3 inhibitors.</p><p><strong>Conclusion: </strong>The Drp1-NLRP3 axis is one of the essential mechanistic connections between mitochondrial dynamics and neuroinflammation in PD. Focusing on this axis could offer novel therapeutic options, and advancing these approaches could pave the way for therapies that not only alleviate symptoms but also slow or halt the progression of the disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Tumor Microenvironment: Impact on Tumor Growth, Metastasis, and Therapeutic Resistance: A Systematic Review.","authors":"Jiazhi Yan, Shuo Tu","doi":"10.2174/0115665240388282250903221303","DOIUrl":"https://doi.org/10.2174/0115665240388282250903221303","url":null,"abstract":"<p><strong>Introduction: </strong>This systematic review assesses the role of the tumor microenvironment (TME) in cancer progression and therapy resistance by defining drug-microenvironment interactions and determining the molecular determinants in the TME that could help improve the efficacy of administered treatments and alleviate existing adverse effects.</p><p><strong>Methods: </strong>This systematic review follows the PRISMA protocol and the PICOS selection framework to retrieve studies from PubMed/MEDLINE, Web of Science, Scopus, and the Cochrane Library. Only original human-related research published in English between 2008 and 2023 was used to explore the reciprocal relation between tumor cells and TME components. The ROBINS-I tool assessed the risk of bias.</p><p><strong>Results: </strong>Out of 258 articles initially identified, 15 met the inclusion criteria for this review. The results showed that TMEs significantly influence treatment outcomes in cancer progression, metastasis, and drug resistance. Focusing on TMEs like CAFs, immune cells, and ECM enhances drug efficacy. The study highlighted potential strategies to improve drug delivery, suppress metastatic processes, and restore immune function, ultimately leading to better outcomes for cancer patients.</p><p><strong>Discussion: </strong>Original evidence suggests that Cancer-Associated Fibroblasts (CAFs), immune cells, and Extracellular Matrix (ECM) contribute to therapeutic resistance and metastasis within the TME. They also promote metastasis by inducing Epithelial- Mesenchymal Transition (EMT) and affecting Cancer Stem Cell (CSC) populations. Moreover, the immunosuppressive TME consists of regulatory T cells and myeloidderived suppressor cells that allow tumors to evade the immune system, a concern for immunotherapy.</p><p><strong>Conclusion: </strong>The TME plays a vital role in cancer development, metastasis formation, and therapy failure. The perspectives for innovative ECM-modulating treatments and interventions targeting the direct interactions between TME and cancer cells can be revolutionary and suggest better outcomes for treatment-naïve and refractory cancers. Future research should use these results as inputs to apply clinical and therapy studies to enhance cancer management outcomes.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Novel Combined Therapeutic Approach to Endometriosis: Exosomes Derived from Human Wharton's Jelly Mesenchymal Stem Cells and Etanercept.","authors":"Roya Mahdavi, Dian Dayer, Afshin Amari, Zorvan Jalili, Mehri Ghafourian, Maryam Farzaneh","doi":"10.2174/0115665240386032250914233540","DOIUrl":"https://doi.org/10.2174/0115665240386032250914233540","url":null,"abstract":"<p><strong>Introduction: </strong>Endometriosis is a chronic disorder characterized by abnormal endometrial tissue growth. This study evaluates a novel combination immunomodulatory treatment involving etanercept (ETN) and exosomes derived from human Wharton's jelly mesenchymal stem cells (hWJMSC-Exo) as a promising alternative to conventional therapies for modulating inflammation in endometriosis.</p><p><strong>Methods: </strong>Endometrial stromal cells were isolated by enzymatic digestion of eutopic (EuESCs, N = 6) and ectopic (EESCs, N = 6) tissues of endometriosis patients and non-endometriotic controls (CESCs, N = 6). hWJMSC-Exo were confirmed by flow cytometry, SEM, and DLS tests. Cells were treated with varying concentrations of ETN (0-40 μg/ml), hWJMSC-Exo (0-15 μg/ml), and their combination (E+E). IC50 values were determined using the MTT assay at 24, 48, and 72 hours. Protein levels of TNF- α, VEGF-A, and IL-10, and gene expression of MMP-2, MMP-9, MCP-1, aromatase, TSLP, and TGF-β1 were measured using ELISA and RT-PCR, respectively.</p><p><strong>Results: </strong>The combination of ETN (10 μg/ml) and hWJMSC-Exo (10 μg/ml) at 24 and 48 hours, respectively, reduced protein expression of TNF-α, VEGF-A, and IL-10 in EESCs, EuESCs, and CESCs compared with untreated groups (P < 0.001). Additionally, E+E treatment significantly reduced mRNA expression of MMP-2, MMP-9, MCP-1, aromatase, TSLP, and TGF-β1 in all three groups compared to untreated groups.</p><p><strong>Discussion: </strong>This combination therapy improves inflammation, angiogenesis, tissue remodeling, and immune regulation in endometriosis. However, clinical validation and long-term safety require further in vivo studies with larger sample sizes.</p><p><strong>Conclusion: </strong>E+E treatment synergistically reduced key cytokines and enzymes in endometriosis. This approach is a promising means of regulating inflammation.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145136660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.","authors":"Roya Mahdavi, Zahra Akbari Jonoush, Nastaran Mohammadi, Abdolah Mousavi Salehi, Nooshin Ghadiri, Mahtab Sayadi, Mahmoodreza Behravan, Farideh Moramezi, Mehri Ghafourian, Maryam Farzaneh","doi":"10.2174/0115665240393552250908133211","DOIUrl":"https://doi.org/10.2174/0115665240393552250908133211","url":null,"abstract":"<p><p>Endometriosis is a typical disorder affecting the female reproductive system and is characterized by the presence of tissue resembling the endometrium both within and beyond the pelvic cavity. Unfortunately, the etiology of endometriosis is not well understood. The purpose of this document is to create a summary of the factors contributing to endometriosis, especially the dysregulation of cellular and molecular pathways. Key biological processes implicated include enzyme dysregulation, exosome dysfunction, hormonal imbalances, apoptosis, angiogenesis, oxidative stress, epigenetic dysregulation, and the involvement of cytokines and chemokines. Many of these factors have overlapping pathways that can enhance the survival of endometrial debris and facilitate the implantation of endometrial tissue in extrauterine sites. This knowledge can provide a broader perspective on the onset and progression of endometriosis. Additionally, this study paves the way for the discovery of new therapeutic targets to improve the efficacy of endometriosis treatments and reduce the side effects associated with current treatments. Further research is needed to better understand the underlying mechanisms that lead to the dysregulation of diseaserelated pathways, which could ultimately be useful in early diagnosis and disease staging.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}