Current molecular medicine最新文献

{"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":"Association Between Bilirubin and Klotho Levels in US Middleaged and Older Adults: NHANES 2007-2016.","authors":"Cunbao Ling, Libing Tian, Jielei Sun, Yuxin Yin, Xiumei Cheng","doi":"10.2174/0115665240425215251212075747","DOIUrl":"https://doi.org/10.2174/0115665240425215251212075747","url":null,"abstract":"<p><strong>Objective and methods: </strong>Bilirubin, a potent endogenous antioxidant, protects against multiple diseases. This cross-sectional study explored the relationship between Serum Total Bilirubin (STB) and Serum Klotho (S-Klotho, an anti-aging biomarker) in 40-79-year-olds from the 2007-2016 NHANES survey. Statistical analysis used a multivariable regression model; a Restricted Cubic Spline (RCS) model evaluated potential non-linear STB-S-Klotho associations. Subgroup analyses and sensitivity tests ensured the robustness.</p><p><strong>Results: </strong>The analysis included 4,562 individuals aged 40-79. Both unadjusted and adjusted models showed a significant positive association between STB and S-Klotho (β = 2.84, P = 0.02 in the weighted, fully adjusted model). The RCS curve indicated no significant non-linearity (P for non-linearity = 0.211). Subgroup analyses revealed stronger associations in females, normal-weight individuals, and those without diabetes mellitus (DM) or hypertension.</p><p><strong>Discussion: </strong>This is the first study exploring the STB-S-Klotho relationship. While human studies on bilirubin's role in aging have inconsistent conclusions, animal and mechanistic research show that elevated bilirubin reduces oxidative stress and inflammation, potentially protecting against age-related conditions.</p><p><strong>Conclusion: </strong>Our findings confirm a positive STB-S-Klotho correlation in middle-aged and older adults, suggesting bilirubin may be a potential S-Klotho biomarker and reflect biological aging processes.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834706","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}

{"title":"Effect of hucMSC-derived Exosomes on the Pressure Ulcers in Mice.","authors":"Fei Yan, Junzheng Yang, Meihua Gong, Guangheng Li, Li Yu","doi":"10.2174/0115665240450312260206114749","DOIUrl":"https://doi.org/10.2174/0115665240450312260206114749","url":null,"abstract":"<p><strong>Introduction: </strong>Pressure ulcers (PUs) are a result of sustained compression of the local skin, leading to impaired blood circulation and subsequent nutritional deficiencies in the skin and subcutaneous tissues. Exosomes are one type of extracellular vesicle with a size range of 40 to 160 nm. Currently, the effects of Human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-exos) on the PUs and the underlying mechanisms remain largely unexplored.</p><p><strong>Methods: </strong>In this study, a PUs model was constructed using BALB/c mice, and the effect of hucMSC-exos on the PUs mice was evaluated by using histopathological examination, quantitative real-time polymerase chain reaction (qRT-PCR), and western blotting.</p><p><strong>Results: </strong>The results of HE staining and Masson staining demonstrated that the treatment of hucMSC-exos could alleviate the histopathological changes of mice. Furthermore, the results of qPCR demonstrated that hucMSC-exos decreased the levels of collagen I, collagen III, and α-SMA in PUs mice; and the results of western blotting demonstrated that the expressions of HMGB1 and α-SMA could be decreased by the administration of hucMSC-exos.</p><p><strong>Discussion: </strong>The data in the manuscript suggest that hucMSC-exos are both safe and effective in the treatment of PUs. It is recommended that large-scale animal experiments and long-term administration time of hucMSC-exos should be conducted to further verify the effect of hucMSC-exos in PUs.</p><p><strong>Conclusion: </strong>The findings of this study demonstrated that hucMSC-exos alleviated the symptoms of PU mice by regulating HGMB1 and α-SMA, thus demonstrating the therapeutic potential of hucMSC-exos in PUs.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147765168","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":"Sulfur Dioxide Inhibits TNF-α-induced Photoreceptor Cell Apoptosis Through Sulfenylation of Caspase-3 at Cysteine 163.","authors":"Jiantong Du, Yaqian Huang, Kun Li, Xiaoqi Yu, Boyang Lv","doi":"10.2174/0115665240478494260327203818","DOIUrl":"https://doi.org/10.2174/0115665240478494260327203818","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Photoreceptor cell apoptosis contributes significantly to vision loss in retinal degenerative diseases. Gasotransmitter sulfur dioxide (SO2) has been implicated in the regulation of apoptotic processes. This study investigated changes in the endogenous SO2/aspartate aminotransferase (AAT) system during tumor necrosis factor-α (TNF-α)-induced photoreceptor cell apoptosis.</p><p><strong>Methods: </strong>We examined the effect of endogenous SO2 on the TNF-α-stimulated apoptosis in 661 W photoreceptor cells and investigated the underlying molecular mechanisms. TNF-α-stimulated 661 W photoreceptor cells served as a cellular model to assess apoptosis via a TdT-mediated dUTP nick-end labeling (TUNEL) assay. We evaluated caspase-3 activation using western blotting and quantified its activity using a colorimetric assay. Site-directed mutagenesis and biotin-switch assays were performed to detect the effects of caspase-3 sulfenylation.</p><p><strong>Results: </strong>During TNF-α-induced apoptosis in photoreceptor cells, the endogenous SO₂ system was markedly upregulated, which correlated with the effective inhibition of apoptosis. SO2 directly suppresses caspase-3 activity in retinal photoreceptor cells and recombinant proteins. Importantly, site-directed mutagenesis revealed that the C163S mutation in caspase-3 abolished SO2-mediated sulfenylation, thereby reducing its anti-apoptotic effects. These findings indicate that endogenous SO2 exerts its protective effects by sulfenylating caspase-3 at cysteine 163.</p><p><strong>Discussion: </strong>Our study demonstrates that upregulation of the endogenous SO2 system directly inhibits caspase-3 activation through sulfenylating cysteine 163 in caspase-3, effectively reducing TNF-α-induced apoptosis in 661 W cells. These findings highlight the precise regulatory role of SO2 in apoptosis.</p><p><strong>Conclusion: </strong>This study provides novel insights into potential therapeutic targets for retinal degenerative diseases.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147671019","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":"Network-based Transcriptomic Profiling of Fetal Astrocyte Differentiation Reveals Therapeutic Targets for Neurodegenerative Disease.","authors":"Arya Moftakhar-Bazkiaei, Maryam Farzaneh","doi":"10.2174/0115665240412373260224061022","DOIUrl":"https://doi.org/10.2174/0115665240412373260224061022","url":null,"abstract":"<p><strong>Introduction: </strong>Neurodegenerative disorders, including Alzheimer's Disease (AD), Parkinson's Disease (PD), and Age-related Macular Degeneration (AMD), are marked by the progressive loss of specific neuronal populations. Astrocytes, the glial cells surrounding neurons, play a critical role in maintaining neuronal health by providing neurotrophic support, producing antioxidants, and clearing waste. Dysfunctional astrocytes contribute to disease progression, yet their developmental trajectory and molecular regulation remain incompletely understood.</p><p><strong>Method: </strong>This study aims to computationally characterize transcriptional differences between fetal astrocytes and neural stem cell lines to identify key regulatory genes, pathways, and therapeutic targets relevant to astrocyte-linked neurodegeneration. Using microarray data and bioinformatics pipelines, 359 Differentially Expressed Genes (DEGs) were identified, including 249 upregulated and 110 downregulated transcripts.</p><p><strong>Results: </strong>Protein-Protein Interaction (PPI) network analysis revealed ten hub genes- COL1A1, TIMP1, LOX, COL6A1, COL6A3, COL5A1, CD44, LTBP2, ACTA2, and PLAU-central to extracellular matrix remodeling and cell adhesion. Drug-gene interaction analysis linked these genes to compounds such as Estradiol valerate, Retinoic acid, and Calcitriol, suggesting therapeutic relevance.</p><p><strong>Discussion: </strong>Enrichment analysis highlighted transcriptional regulation, apoptosis, and ECM-receptor interaction as dominant biological themes. Key miRNA-mRNA interactions, including hsa-miR-877-5p and hsa-miR-767-5p targeting LOX and COL6A3 were also identified.</p><p><strong>Conclusion: </strong>Overall, this study integrates transcriptomic profiling, network modeling, and drug-gene interaction analysis to uncover astrocyte-specific molecular targets, offering a computational framework for therapeutic exploration in neurodegenerative disease.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147618535","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":"Overexpression of Membrane Metalloendopeptidase Attenuates Oxidative Stress and Inflammation in Diabetic Neuropathy via the Nrf2/HO-1 Pathway.","authors":"Zenghui Liu, Jianlin Ge, Jiafeng Sun, Xuefeng Yang, Qian Su, Xin Sun, Boxiang Du","doi":"10.2174/0115665240406476260220084033","DOIUrl":"https://doi.org/10.2174/0115665240406476260220084033","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the role of Membrane Metalloendopeptidase (MME) in oxidative stress and inflammation in painful diabetic neuropathy, and to explore the underlying mechanism.</p><p><strong>Methods: </strong>A diabetic mouse model was established with streptozocin (STZ) injections. Neuropathic pain was assessed using paw withdrawal latency (PWL). Target genes related to painful diabetic neuropathy were identified using the Comparative Toxicogenomic Database (CTD), DisGeNET, and GeneCards. Protein-protein interactions between MME and the Nrf2/HO-1 signaling pathway were analyzed using the String database. The effects of MME overexpression, with or without the Nrf2 inhibitor ML385, on neuropathy were examined. Blood glucose, insulin levels, oxidative stress indicators, and inflammatory cytokines were measured. Gene expression was quantified by qRT-PCR, and protein levels were assessed by Western blot and immunohistochemistry.</p><p><strong>Results: </strong>Diabetic mice showed elevated blood glucose, MDA, ROS, TNF-α, IL-1β, IL-6, and decreased serum insulin, PWL, SOD activity, and MME levels. MME interacted with Nrf2 and HO-1, which were reduced in diabetic mice. Overexpression of MME led to improved serum insulin, PWL, SOD activity, and increased Nrf2 and HO-1 levels, while reducing MDA, ROS, TNF-α, IL-1β, and IL-6. These effects were partially reversed by ML385.</p><p><strong>Conclusion: </strong>Overexpression of MME mitigates oxidative stress and inflammation in painful diabetic neuropathy by activating the Nrf2/HO-1 signaling pathway.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607830","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":"Gut Microbiota and Metabolic Profiles Reveal the Mechanism of Weight Loss in Patients with Obesity Stimulated By Acupuncture.","authors":"Yan Huo, Jianfang Gao, Ying Lv, Bingwei Ai","doi":"10.2174/0115665240391524251201102455","DOIUrl":"https://doi.org/10.2174/0115665240391524251201102455","url":null,"abstract":"<p><strong>Introduction: </strong>This study aims to elucidate the mechanisms underlying the efficacy of Quantitative Lifting And Inserting Acupuncture (QLIA) in treating simple obesity through integrated metabolomic and gut microbiota analyses.</p><p><strong>Methods: </strong>Thirty patients with obesity were randomized into treatment (QLIA), control (standard needle lifting), and healthy groups (standard needle lifting) (n=10 each). Acupuncture was administered three times per week for 8 weeks. 16S rRNA sequencing was performed on fecal samples, and serum samples were analyzed using ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLCMS/ MS) metabolomics.</p><p><strong>Results and discussion: </strong>QLIA significantly altered gut microbiota α-diversity and β- diversity. The Firmicutes/Bacteroidetes ratio was significantly increased in the QLIAtreated group. The treatment group showed increased abundance of beneficial bacteria such as Bifidobacterium and Dialister, and decreased abundance of potentially harmful bacteria such as Escherichia-Shigella. KEGG pathway analysis revealed upregulation of amino acid biosynthesis and carbohydrate metabolism pathways and downregulation of nucleotide biosynthesis pathways in the gut microbiota. Metabolomic analysis showed significantly elevated levels of acetyl-Lcarnitine and decreased levels of N-acetylneuraminic acid in the treatment group after acupuncture. PICRUSt analysis primarily implicated amino acid metabolic pathways. Serum metabolite analysis identified lipid, carbohydrate, and amino acid metabolism pathways as key targets of acupuncture intervention. Comparative analysis of metabolic pathways revealed amino acid metabolism as a shared target in both gut microbiota and serum metabolite profiles. These findings suggest that QLIA exerts its weight-loss effects by reshaping the gut microbiota structure and modulating host metabolic profiles, thereby highlighting a synergistic mechanism involving the gut-host metabolic axis.</p><p><strong>Conclusion: </strong>QLIA significantly promoted weight loss in simple obesity by modulating key metabolic pathways and altering gut microbiota composition. The study provides insight into the mechanisms underlying acupuncture-induced weight loss and supports its potential as a therapeutic option for obesity.</p>","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147607871","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 MicroRNA-200 Family in Gastrointestinal Cancers.","authors":"Jun Li, Jinling Pan, Jinjun Wen, Chuan Wang","doi":"10.2174/0115665240440515260204045401","DOIUrl":"https://doi.org/10.2174/0115665240440515260204045401","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Gastrointestinal cancers, including esophageal cancer, gastric cancer, liver cancer, pancreatic cancer, and colorectal cancer, are a major health burden worldwide, characterized by high incidence and mortality rates. Traditional diagnostic methods are not satisfactory. The compliance of patients with endoscopic examinations is poor, and the sensitivity and specificity of conventional tumor markers are also not high. Liquid biopsy, especially the detection of exosomal microRNAs (miRNAs), as a promising alternative method, has emerged, among which the miR-200 family has been identified as a key regulatory factor in the pathogenesis of gastrointestinal cancers.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;A literature search was conducted from 2002 to 2025, and the keywords used included \"gastrointestinal cancer\", \"miR-200 family\", and \"exosomal miRNA\". The studies involved included those on the role of miR-200 in gastrointestinal cancers, as well as research on exosomal miR-200 as a biomarker or therapeutic target. Inclusion criteria include: original studies published in English and peer-reviewed, which explored the biological, diagnostic, prognostic, or therapeutic effects of the miR-200 family in gastrointestinal cancers, and provided the complete papers that are accessible. If the research is a review, a conference summary, an editorial, a duplicate dataset, or lacks sufficient experimental or clinical data related to miR-200, it will be excluded. This literature search was conducted in the PubMed database. After screening, a total of 248 articles were obtained, and finally, 133 studies were included in the analysis. This review adhered to the guidelines of SANRA and employed a narrative research method. The key findings were qualitatively synthesized to summarize the mechanism of miR-200 and its clinical relevance.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;MicroRNA-200 regulates the occurrence and development of gastrointestinal cancers by modulating epithelial-mesenchymal transition (EMT), angiogenesis, cancer stem cell properties, and chemotherapy resistance. Its expression in tumor tissues is closely related to clinical pathological features, prognosis, and treatment response. Furthermore, the miR-200 present in exosomes exhibits extremely high stability in circulation and specificity towards cancer.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Studies have shown that miR-200 family regulates the occurrence and development of gastrointestinal cancer by targeting epithelial-mesenchymal transition, angiogenesis, and other characteristics, and its expression is related to clinicopathological characteristics and prognosis. Exosomal miR-200 family has shown good diagnostic performance in gastrointestinal malignancies. In an independent validation cohort, the AUC of combined miR-200a-3p and miR200b-3p expression in pancreatic ductal adenocarcinoma (PDAC) was 0.97, with a sensitivity of 100% and a specificity of 88%. Notably, combining this miRNA","PeriodicalId":10873,"journal":{"name":"Current molecular medicine","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493675","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}