Current molecular medicine最新文献

{"title":"Pharmacological Mechanisms of Curcumin and Resveratrol in Inflammation-associated Head and Neck Cancer Progression and Pain Management.","authors":"Xinyu Lu, Siyuan Song","doi":"10.2174/0115665240435144251126045042","DOIUrl":"https://doi.org/10.2174/0115665240435144251126045042","url":null,"abstract":"<p><p>Head and Neck Cancer (HNC) represents a significant global health challenge, marked by high incidence, poor prognosis, and frequent association with chronic inflammation. Pain management in HNC is complex and often inadequate. Curcumin and resveratrol, two naturally occurring polyphenols, have attracted considerable attention for their anti-inflammatory and anti-cancer activities. This review systematically examines the molecular mechanisms by which curcumin and resveratrol modulate key signaling pathways, including NF-κB, STAT3, PI3K/Akt/mTOR, and SIRT1, in the context of HNC progression and pain. Curcumin exerts its effects by inhibiting pro-inflammatory cytokines, suppressing tumor proliferation, and inducing apoptosis, while resveratrol activates SIRT1, inhibits MAPK and mTOR pathways, and enhances apoptosis and anti-metastatic effects. Both compounds influence the tumor microenvironment, potentially enhancing anti-tumor immunity. Combined, they may provide synergistic benefits, including augmented apoptosis and enhanced modulation of inflammatory pathways. Preclinical evidence supports their efficacy in tumor suppression and pain reduction, though clinical translation remains limited due to poor bioavailability. Recent advances in nanoformulations have improved systemic delivery, and initial clinical trials show promising effects in reducing oral mucositis and modulating antioxidant status. However, large, well-designed clinical trials are needed to confirm their therapeutic roles, clarify synergistic mechanisms, and optimize formulations for effective HNC treatment. Dedicated research on pain management and opioid-sparing effects is especially warranted. Together, curcumin and resveratrol represent promising adjuncts to current HNC therapies, with the potential to improve tumor control and patient quality of life.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971209","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":"Sodium Ion Channel Active Agent Deltamethrin Induces Cell Apoptosis and Cell Cycle Arrest through Mitochondrial Dependent Pathway in Human Fetal Lung Fibroblasts.","authors":"Xiaohua Wang, Wanlin Shen, Tian Tian, Xingjuan Zhang, Mingxia Yang","doi":"10.2174/0115665240389973251027101544","DOIUrl":"https://doi.org/10.2174/0115665240389973251027101544","url":null,"abstract":"<p><strong>Introduction: </strong>Pulmonary Fibrosis (PF) is a common outcome of many interstitial lung diseases. Sodium ion channels play an important role in maintaining membrane potential, transmitting ion signals across the membrane, and mediating cell proliferation/migration. Deltamethrin (DM) can prevent the closure of voltage-gated sodium ion channels in insect axon membranes. This study aimed to further evaluate the potential effects of DM on Human Fetal Lung Fibroblasts (HFLF).</p><p><strong>Methods: </strong>The characteristic apoptotic changes were also assessed using DNA fragmentation analysis, terminal deoxynucleotidyl Transferase-Mediated Dutp Nick End Labeling (TUNEL), and annexin V/PI and Hoechst 33342/PI double staining. In addition, DM-induced cell cycle arrest in the G0/G1 phase was detected in a dosedependent manner. Furthermore, transcriptional and translational expression of selected genes under DM stress were used to confirm the analysis.</p><p><strong>Results: </strong>We showed that DM dose-dependently decreased cell viability and inhibited cell proliferation in the HFLF cell line. The data suggested that the effect of DM inhibition was at least partly through regulating the expression of Ras, p53, p21, p27, cyclin D1, cytochrome c, caspase-3, and Bcl-2 family members.</p><p><strong>Discussion: </strong>These results revealed that DM might induce cell apoptosis and cell cycle arrest through a mitochondrial-dependent cytotoxic stress pathway in the HFLF cell line, but there is a lack of animal experiments to verify this. We will continue to follow up on the experiment to further improve it.</p><p><strong>Conclusion: </strong>Our study provides insight into assessing the potential anti-pulmonary fibrosis function of DM at the molecular level.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147971234","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":"Recovery Kinetics and Persistent Hepatic Alterations in a Xenobiotic-induced Murine Model of Chronic Cholestatic Liver Disease.","authors":"Mayalen Valero-Breton, Marianny Portal-Rodriguez, Franco Tacchi, Javier Salgado-Valdovinos, Matías Monsalves-Álvarez, Christian Hidalgo, Caroll Stoore, Rodolfo Paredes, Daniel Cabrera, Claudio Cabello-Verrugio","doi":"10.2174/0115665240427841251211110201","DOIUrl":"https://doi.org/10.2174/0115665240427841251211110201","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Chronic cholestatic liver disease (CCLD) is characterized by impaired bile production and excretion due to its inflammatory nature and potential progression to biliary cirrhosis. Murine models mimic cholestatic-type human liver diseases, such as the 3,5- diethoxycarbonyl-1,4-dihydrocholidine (DDC) model. Nonetheless, the timeline for liver regeneration following cessation of the DDC diet remains unclear. This study aimed to evaluate the duration of hepatic alterations after cessation of the DDC diet.</p><p><strong>Methods: </strong>C57BL/6J male mice (16-17 weeks old) were randomly assigned to Control (standard diet) and CCLD (DDC-supplemented diet) groups. After six weeks of diet exposure, the DDC group transitioned to a standard diet. Liver parameters were evaluated at 3-, 18-, and 36-days post-diet cessation. Analysis included liver damage and weight, histopathology, and biochemical markers.</p><p><strong>Results: </strong>Liver damage remained elevated until day 36, whereas liver weight remained elevated until day 18. Histological analysis confirmed that bile duct obstruction and fibrosis scores in the DDC group remained significantly higher than in controls up to 36 days after the DDC diet. Serum bile acid levels remained elevated for up to 18 days, while GGT levels did not differ across time points. AST levels were markedly increased at 3 days, whereas ALT levels remained elevated at 3 and 18 days.</p><p><strong>Discussion/conclusion: </strong>Total cholesterol and triglyceride levels increased until day 18, highlighting changes in lipid metabolism. Our study demonstrates hepatic effects in the DDCinduced CCLD model, with alterations persisting beyond cessation of hepatotoxin exposure. These findings show the temporal dynamics of CCLD after diet cessation through different liver parameters.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940575","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":"Molecular Mechanisms of New and Re-purposed Synthetic as well as Natural Bioactive Molecules Against Breast Cancer: Elucidating Targets, Signaling Pathways, Resistance Modulation, and Synergistic Combinations for Prevention.","authors":"Saptarshi Samajdar, Kazi Julekha, Subhayan Mishra, Deepsa Guhu","doi":"10.2174/0115665240440305260306055108","DOIUrl":"https://doi.org/10.2174/0115665240440305260306055108","url":null,"abstract":"<p><p>Breast cancer remains a major public health challenge in India, with rising incidence and the limited efficacy of conventional chemotherapeutics driven by multidrug resistance (MDR), systemic toxicity, and therapeutic relapse. This review synthesizes emerging mechanistic evidence on repurposed synthetic agents and bioactive natural compounds, presenting a unified framework for mechanism-guided anti-cancer intervention. The selective estrogen receptor modulator (SERM) ormeloxifene exemplifies the promise of drug repurposing, exerting multi-target cytotoxicity through mitochondrial membrane depolarization, G0/G1 cell-cycle arrest, caspase-dependent apoptosis, ERα modulation, and disruption of proliferative signaling circuits. In parallel, potent natural products-including ellagitannins (corilagin, castalin, punicalagin) and triterpenoid saponins (α-hederin, D-rhamnose-β-hederin, quillaic acid, hederagenin)-demonstrate complementary mechanisms by enhancing intracellular ROS accumulation, suppressing PI3K/Akt and mTOR signaling, inhibiting NF-κB activation, and triggering intrinsic and extrinsic apoptotic pathways. Integrating these mechanistic axes, this review highlights a key innovation: both synthetic and phytochemical scaffolds converge on actionable molecular nodes governing survival signaling, metabolic rewiring, and MDR modulation. This convergence underscores their translational potential for developing combination or sequential regimens that enhance selectivity, circumvent drug resistance, and minimize off-target toxicity. Collectively, these mechanistically validated agents represent promising leads for preclinical optimization and rational design of next-generation, pathway-directed breast cancer therapeutics.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940619","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":"Diagnostic and Prognostic Significance of the S100 Biomarker in Blast-related Closed Traumatic Brain Injury.","authors":"Evgenii I Balakin, Kseniya A Yurku, Vasiliy I Pustovoyt","doi":"10.2174/0115665240416190260113093055","DOIUrl":"https://doi.org/10.2174/0115665240416190260113093055","url":null,"abstract":"<p><strong>Introduction: </strong>Traumatic Brain Injury (TBI) is a frequent cause of long‑term disability in service members who have been exposed to blast, and clinicians often lack reliable tools to quantify the actual burden of damage early after injury. Among available candidates, S100B is a calcium‑binding protein of astroglial origin that appears in the bloodstream when the blood-brain barrier is disrupted, and neuronal structures are injured. Its diagnostic and prognostic properties in the specific setting of blast‑related closed TBI, however, remain incompletely defined. The present study, therefore, focuses on military personnel with blast‑related closed TBI and examines the diagnostic and prognostic significance of serum S100 by tracking its concentration at several post‑injury time points across predefined severity groups.</p><p><strong>Methods: </strong>A prospective cohort of military patients with blast‑related closed TBI was examined, and serum S100 concentrations were measured at 1, 3, 6, and 12 hours after injury. Patients were stratified into mild, moderate, and severe TBI categories, and S100 dynamics were analysed in relation to these severity groups using standard descriptive statistics, group‑comparison tests, ROC analysis, correlation analysis, and K‑means clustering, as detailed in the Methods section.</p><p><strong>Results: </strong>Serum S100 levels peaked at 6 hours after trauma and showed a moderate correlation with TBI severity (r = 0.65, p < 0.001). Statistically significant differences in S100 concentrations were found between severity groups at all investigated time points (p < 0.001), and ROC analysis yielded an AUC of 0.81 for severity discri-mination. Diagnostic performance indices (AUC, optimal cutoff, sensitivity, specificity, positive and negative predictive values, and overall accuracy with 95% confidence intervals) are summarised in the Results, and K‑means clustering revealed distinct patient subgroups with different temporal S100 profiles, indicating the feasibility of more personalized risk stratification and management.</p><p><strong>Discussion: </strong>These findings support the use of S100 as a clinically relevant biomarker for early grading of blast‑related closed TBI and short‑term outcome prediction. Incorporating S100 into multimodal assessment algorithms may improve risk stratification and guide timely therapeutic decisions in affected patients.</p><p><strong>Conclusion: </strong>S100 can be considered a useful biomarker for early grading of brain injury severity and outcome prediction in blast‑related closed TBI. Integration of S100 into multimodal diagnostic algorithms has the potential to improve stratification of patients, inform therapeutic decision‑making, and enhance outcomes in military and civilian populations exposed to blast trauma.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940553","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":"Effects of 1,8-Cineole on Diabetic Muscular Atrophy.","authors":"Laiali T Al-Quraan, Bahaa Al-Trad, Ghada Alomari, Alaa A A Aljabali, Aseel Al-Shwaheen","doi":"10.2174/0115665240427156260213154744","DOIUrl":"https://doi.org/10.2174/0115665240427156260213154744","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to address the effects of 1,8-cineole on diabetic muscular atrophy in streptozotocin (STZ)-induced diabetic rats.</p><p><strong>Materials and methods: </strong>Adult male rats were divided into three groups (n = 15): nondiabetic control (ND), diabetic (D), and diabetic rats treated with 1,8-cineole intraperitoneally for 21 days. A single low-dose intraperitoneal injection of STZ (50 mg/kg) was used to induce diabetes. At the end of the experiment, blood and muscle tissue samples were collected for analysis.</p><p><strong>Results: </strong>There was a significant increase in blood glucose levels in diabetic rats, which coincided with significant increases in the skeletal muscles' mRNA expression levels of two inflammatory markers, transforming growth factor-β1 (TGF-β1) and tumor necrosis factor-α (TNF‑α), and in two biomarkers of skeletal muscle atrophy, F-boxonly protein 32 (FBXO32) and muscle RING-finger protein-1 (MuRF1). Additionally, diabetic rats showed a significant decrease in the expression of skeletal muscle glucose transporter 4 (GLUT4) levels. The malondialdehyde (MDA) level was increased, while the activity of superoxide dismutase (SOD) was not changed in the skeletal muscle of the D group compared to the ND group. Cineol treatment reversed the diabetes-induced changes in the relative mRNA expression levels of TGF-β1, TNF- α, FBXO32, MuRF1, and GLUT4 in the skeletal muscle and significantly decreased MDA levels with a non-significant increase in skeletal muscle SOD activity.</p><p><strong>Discussion: </strong>These results suggest that 1,8-cineole protects diabetic skeletal muscles in multiple ways, including reducing oxidative stress, inhibiting the generation of inflammatory cytokines, and preventing the expression of proteolytic genes. Its capacity to increase GLUT4 levels enhances glucose absorption and insulin sensitivity. Therefore, in diabetic situations, 1,8-cineole may help maintain muscle structure and function. These findings add to the increasing amount of data indicating that 1,8- cineole is a viable option for treating diabetes-induced muscle problems brought on by diabetes. To fully understand its therapeutic potential, further research is necessary, including studies on muscle mass, myostatin levels, and protein expression.</p><p><strong>Conclusion: </strong>1,8-cineole tr1eatment decreased blood glucose levels and attenuated oxidative stress and inflammation in the skeletal muscles of diabetic rats, thereby protecting rats against diabetic muscle atrophy.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940608","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 Pathological Development of EndMT in Lung Diseases and its Regulatory Mechanisms.","authors":"Jingqian Huang, Pengxiang Wang, Yiting You, Yujian Liu, Xiaochen Bao, Xiaoyan Zhu","doi":"10.2174/0115665240408525251203054415","DOIUrl":"https://doi.org/10.2174/0115665240408525251203054415","url":null,"abstract":"<p><p>Endothelial-to-Mesenchymal Transition (EndMT) is a regulatory mechanism integral to the normal developmental processes of the organism, playing a pivotal role in sustaining the homeostasis of the intravascular milieu. However, when the internal environment exceeds the endothelium's compensatory capacity, excessive EndMT can precipitate pathological alterations. EndMT is particularly significant in the pathogenesis of pulmonary diseases, including pulmonary fibrosis, pulmonary hypertension, and lung cancer. The regulatory mechanisms underlying EndMT are intricate and multifaceted. Numerous signaling pathways have been implicated in EndMT modulation, with the TGF-β pathway emerging as a central inducer. Furthermore, research has identified that epigenetic modifications, metabolic processes, hypoxia, inflammatory cytokines, and oxidative stress all contribute to the regulation of EndMT. This complexity renders the interplay between EndMT and pulmonary vascular diseases exceedingly intricate. In this manuscript, we provide a comprehensive overview of the signaling pathways and other influencing factors that govern EndMT. Concurrently, we meticulously delineate potential therapeutic targets to offer novel avenues and insights for the management of pulmonary diseases. Our synthesis of the current understanding of EndMT regulation is intended to inform future research and clinical strategies, potentially leading to more effective interventions for patients afflicted with pulmonary disorders.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147940611","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 Effect of mascRNA on the Phenotype Transition and Mitophagy in Vascular Smooth Muscle Cells Exposed to Hypoxia.","authors":"Jingyuan Hou, Ruiqiang Weng, Xia Li, Xiaodong Gu, Junli Zhao, Sudong Liu","doi":"10.2174/0115665240427492251210155520","DOIUrl":"https://doi.org/10.2174/0115665240427492251210155520","url":null,"abstract":"<p><strong>Introductions: </strong>A primary complication of atherosclerosis(AS) is characterized by chronic inflammatory and mitochondrial dysfunction, both of which play critical roles in the disease's progression. This study aims to investigate the regulatory role of mascRNA in mediating the hypoxia-induced phenotypic transition of vascular smooth muscle cells (VSMCs).</p><p><strong>Methods: </strong>An AS model was established, and the aortic plaque area was assessed by Oil Red O staining. Human VSMCs were divided into five groups: normoxia, hypoxiainduced, negative control (pGV-NC), mascRNA overexpression (pGV-mascRNA), and inhibitor-treated. Quantitative PCR (qPCR) was utilized to detect the expression of mascRNA, vWF, and MMP2. Western blotting was performed to detect the expression of phenotypic transformation-related proteins.</p><p><strong>Results and discussion: </strong>In high-fat diet (HFD)-fed mice, the expression of mascRNA was significantly decreased in the aortas (P < 0.05). Hypoxia led to a reduction in mascRNA levels, an upregulation of synthetic markers, and increased reactive oxygen species (ROS) in VSMCs. Overexpression of mascRNA suppressed VSMC migration and proliferation, enhanced mitophagy, and inhibited the PI3K-AKT pathway. Our study has been the first to demonstrate mascRNA play a crucial role in VSMC phenotypic transformation and functions via regulation of mitophagy. These findings highlight mascRNA's role in AS development and provide a theoretical basis for its clinical applications, but in vivo experiments are called for to validate its anti-AS effect.</p><p><strong>Conclusion: </strong>MascRNA suppressed hypoxia-induced phenotypic transformation of VSMCs, potentially through the modulation of the PI3K-AKT signaling pathway and the enhancement of mitochondrial autophagy. These findings indicate a prospective therapeutic application of mascRNA in AS.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834732","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":"Apolipoprotein A2 Influences ANGPTL3 in Modulating TG Catabolism and Inflammatory Cytokines Secretion.","authors":"Ye Cheng, Sicen Wang","doi":"10.2174/0115665240393602260214143040","DOIUrl":"https://doi.org/10.2174/0115665240393602260214143040","url":null,"abstract":"<p><strong>Introduction: </strong>Apolipoprotein A2 (ApoA2) and ANGPTL3 modulate LPL activity and inflammatory cytokine secretion, resultantly influencing TG metabolism and inflammatory response. However, any associations that exist between those modulators were not explored. The study aimed to elucidate the functions of ApoA2 in modulating ANGPTL3 on the metabolism of TG and inflammatory cytokine secretion.</p><p><strong>Method: </strong>A case-control hospital-based clinical study was conducted. A total of 50 patients with diagnosed CAD and 50 healthy control individuals were enrolled. Levels of ApoA2, ANGPTL3, and several pro-inflammatory cytokines were measured.</p><p><strong>Result: </strong>The levels of ANGPTL3 and ApoA2 exhibited no significant discordance between the CAD group and control group. Both ANGPTL3 and ApoA2 were associated with TG (r = 0.249, P = 0.002; r = 0.379, P = 0.001, respectively). Additionally, ApoA2 were inversely associated with hs-CRP (r = -0.079, P =0.003), TNF-α (r = -0.119, P = 0.001), and IL-1β (r = -0.103, P = 0.004). Regression analysis confirmed that ApoA2 was an independent modulator of TG and inflammatory cytokines independent of ANGPTL3 (standardized β = 0.196, P < 0.001).</p><p><strong>Discussion: </strong>ANGPTL3 and ApoA2 correlate with TG levels, with ApoA2 identified as an independent contributor via stepwise regression, and ANGPTL3 exerts its TGregulating effect mainly by inhibiting LPL activity through multiple mechanisms, suggesting its potential anti-inflammatory role, though conflicting findings in existing studies indicate the need for further clarification of this relationship.</p><p><strong>Conclusion: </strong>ApoA2 influences ANGPTL3 in modulating catabolism of TG and atherosclerotic-related inflammatory cytokines, suggesting a vital role of ApoA2 in promoting pathological progression of CAD.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834522","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":"Beyond Conventional Therapy: A Comprehensive Review of Herbal, Traditional, and Emerging Interventions for Polycystic Ovary Syndrome.","authors":"Shafia Bashir, Insha Mushtaq Shah, Shazia Javeed, Aneeqa Rafiquee, Bisma Mir, Reyaz Hassan Mir, Mohammad Ishaq Geer, Mohammad Ashraf Ganie","doi":"10.2174/0115665240406897251206074722","DOIUrl":"https://doi.org/10.2174/0115665240406897251206074722","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is the most common and multifactorial endocrine disorder that leads to significant changes in the reproductive, metabolic, and psychological domains of women's health in their reproductive years. In addition, the conventional therapies (lifestyle modification, metformin, oral contraceptives, and ovulation-inducing agents) that are the mainstay of management of the syndrome may still not be able to fully address the diverse pathophysiology of PCOS as well as the long-term risks associated with it. This narrative review highlights clinical and mechanistic data from studies on various complementary and alternative medicine (CAM) modalities as first-line treatments for PCOS, in addition to conventional therapy. Correspondingly, herbal and botanical agents (berberine, cinnamon, licorice, Vitex agnus-castus, curcumin, and epigallocatechin gallate) modulate insulin signalling, androgen synthesis, inflammatory pathways, and oxidative stress, with initial clinical trials reporting improvements in metabolism and hormones to a similar extent as standard therapies in selected populations. Traditional Chinese Medicine (TCM), both multi-herb prescriptions and acupuncture, provides tailored formulas that might not only regulate ovulation and endocrine parameters but also lower metabolic indices, despite the high variability across studies. Stress reduction, physical fitness, and the quality of life are among the achievements of mind-body interventions (yoga, tai chi, qigong, and mindfulness-based stress reduction). Improvements in hyperinsulinemia, hypolipidemia, ovulation, and hyperandrogenemia, along with the related insulinresistant and vitamin D-deficient phenotypes, have been steadily reported with the use of the nutraceutical combinations of inositols, vitamin D, omega-3 fatty acids, Nacetylcysteine, coenzyme Q10, and resveratrol. New non-conventional methods, such as fecal and vaginal microbiota transplantation, platelet-rich plasma, and kisspeptin analogues, have been identified as potential therapeutic routes but are still in their infancy in terms of development. Although CAM therapies have multiple advantages in controlling many PCOS domains, the official integration into clinical practice would require standardization, rigorous randomized controlled trials, and continuous safety monitoring. If correctly and cautiously applied, CAM may be useful as an adjunct alongside established therapy, rendering PCOS management more holistic and personalized.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834655","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}