International journal of molecular medicine最新文献

{"title":"Exercise training for myocardial ischemia reperfusion injury: Mechanism and clinical practice (Review).","authors":"Junwei Gao, Lingyao Li, Siqi Zhai, Yan Dong, Zhiyi Zhang, Duomao Lin, Jun Ma","doi":"10.3892/ijmm.2025.5632","DOIUrl":"10.3892/ijmm.2025.5632","url":null,"abstract":"<p><p>Myocardial ischemia reperfusion injury (MIRI) remains a key and difficult issue in the field of cardiovascular diseases, and its pathogenesis involves multiple aspects. Exercise can effectively improve MIRI, and the mechanisms include reducing oxidative stress and inflammatory responses, regulating mitochondrial function and metabolic abnormalities, and so on. For patients undergoing reperfusion, rehabilitation therapy mainly based on exercise has important clinical significance. The present study expounded on the occurrence of MIRI from the perspective of mechanisms and the improvement effect of exercise on MIRI, elaborates on the main current exercise strategies and existing problems from the aspect of clinical practice, and discusses the possible future development directions.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanosensor Piezo1‑mediated smooth muscular cell pyroptosis contributes to vascular calcification.","authors":"Jun Tao, Daiting You, Zejiang Feng, Huangjing Li, Yao Zhang, Yuting Cui, Kaiyuan Lin, Bin Luo, Shengli Yin, Hongmei Tan","doi":"10.3892/ijmm.2025.5637","DOIUrl":"10.3892/ijmm.2025.5637","url":null,"abstract":"<p><p>Vascular calcification is a pathological consequence of chronic inflammation and phenotypic switching in smooth muscle cells (SMCs). However, the mechanisms underlying vascular calcification remain unclear. The present study explores the role of the mechanosensor channel, Piezo1, in regulating vascular SMC (VSMC) death and vascular calcification. The findings of the present study demonstrated that Piezo1 expression is upregulated in the atherosclerotic plaques of both mice and patients. <i>In vitro</i> experiments revealed that calcifying medium (CM) induced an increase in Piezo1 and runt‑related transcription factor 2 (RUNX2) expression, triggered pyroptosis in cultured VSMCs and promoted calcium deposition in arterial rings. These effects were mitigated by a Piezo1 inhibitor and exacerbated by a Piezo1 agonist. Furthermore, gene deletion of NLR family pyrin domain containing 3 (NLRP3), caspase1 or gasdermin D also reduced CM‑induced pyroptosis and calcium deposition in VSMCs. Immunoprecipitation assays showed that calcium/calmodulin dependent protein kinase II (CaMKII), a downstream effector of Piezo1, interacted with RUNX2, and CaMKII inhibition attenuated both pyroptosis and calcification in VSMCs exposed to CM. The role of Piezo1 in mediating VSMC pyroptosis and vascular calcification was confirmed in a mouse model, where VSMC‑specific deletion of Piezo1 inhibited arterial calcification in chronic kidney disease. In conclusion, Piezo1 is a key regulator of vascular calcification via Ca2+‑CaMKII‑mediated activation of the NLRP3 inflammasome and subsequent VSMC pyroptosis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] S100A8‑targeting siRNA enhances arsenic trioxide‑induced myeloid leukemia cell death by down‑regulating autophagy.","authors":"Liangchun Yang, Minghua Yang, Hong Zhang, Zhuo Wang, Yan Yu, Min Xie, Mingyi Zhao, Liying Liu, Lizhi Cao","doi":"10.3892/ijmm.2025.5622","DOIUrl":"10.3892/ijmm.2025.5622","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the western blots shown in Fig. 4C, the two left lanes in the 'Fibrillarin' gel slice appeared to be strikingly similar to the mirrored two right lanes in the 'Actin' gel slice, albeit the orientations of the blots were horizontally reversed, such that data which were intended to have shown the results of differently performed experiments appeared to have been derived from the same original source. Moreover, the control β-actin blots featured in Fig. 5A of the above paper were strikingly similar to control blots used in a different context that appeared in a subsequently published paper featuring some of the same authors in <i>American Journal of Cancer Research</i>. The authors were contacted by the Editorial Office to offer an explanation for the apparent anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 29: 65‑72, 2012; DOI: 10.3892/ijmm.2011.806].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological inhibition of casein kinase II attenuates metaflammation in a murine model of diet‑induced metabolic dysfunction.","authors":"Elisa Porchietto, Eleonora Aimaretti, Giacomo Einaudi, Gustavo Ferreira Alves, Debora Collotta, Enrica Marzani, Leonardo Camillò, Chiara Rubeo, Raffaella Mastrocola, Natasha Irrera, Manuela Aragno, Carlo Cifani, Massimo Collino","doi":"10.3892/ijmm.2025.5616","DOIUrl":"10.3892/ijmm.2025.5616","url":null,"abstract":"<p><p>Kinases are activators of well‑known inflammatory cascades implicated in metabolic disorders, and abnormal activation of casein kinase II (CK2) is associated with several inflammatory disorders. However, thus far, its role in the low‑grade chronic inflammatory response known as 'metaflammation', which is a hallmark of obesity and type 2 diabetes, has not yet been elucidated. The present study aimed to evaluate the role of CK2 in diet‑induced metaflammation and the effects of the CK2 inhibitor 4,5,6,7‑tetrabromobenzotriazole (TBB) on a murine model fed a high‑fat‑high‑sugar (HFHS) diet. C57BL/6JOlaHsd mice were fed a standard diet (n=12) or HFHS diet (n=24) for 12 weeks. A subgroup of the HFHS group received TBB (2.5 mg/kg/day, orally, n=12) for the last 8 weeks. Subsequently, plasma and liver samples were harvested for <i>ex vivo</i> biomolecular analyses (immunohistochemistry, western blotting, multiplex assay to determine the plasma levels of pro‑inflammatory cytokines, reverse transcription‑quantitative PCR and enzymatic assays) Statistical significance was determined using one‑way ANOVA with post‑hoc analysis (P<0.05). The results revealed that HFHS feeding induced glucose and lipid intolerance, elevated circulating pro‑inflammatory cytokines and increased hepatic neutrophil infiltration. By contrast, TBB treatment improved glucose and lipid homeostasis, and reduced systemic inflammation without altering body weight. Notably, TBB attenuated hepatic inflammation, reduced neutrophil recruitment and suppressed HFHS‑induced CK2α hyperactivation. This was accompanied by modulation of key inflammatory pathways, including NFκB/nucleotide‑binding domain, leucine‑rich‑containing family, pyrin domain‑containing‑3 and AMPK signaling. In conclusion, the present study demonstrated the beneficial effects of pharmacological inhibition of CK2 in a murine model of diet‑induced metabolic dysfunction, identifying CK2 as a potential target for dampening metaflammation. The efficacy of TBB in relieving hepatic inflammation was mainly due to the interference with selective inflammatory pathways.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of sesamin on the chemosensitivity, invasiveness and immune evasion mechanism of human lung adenocarcinoma.","authors":"Chia-Chia Chao, Pei-Wen Peng, Yen-You Lin, An-Chen Chang","doi":"10.3892/ijmm.2025.5635","DOIUrl":"10.3892/ijmm.2025.5635","url":null,"abstract":"<p><p>Lung adenocarcinoma (LUAD) is a major cause of cancer‑related mortality worldwide. Sesamin is a lignan with potent anticancer properties and promising therapeutic potential. In the present study, it was aimed to investigate the specific mechanisms through which sesamin reduces cell invasiveness and cancer‑associated immunosuppression in LUAD cells. The effects of sesamin on LUAD cell invasiveness were investigated using a wound healing assay and anoikis resistance assay. NK‑92 MI cells were used to analyze cancer‑associated immunosuppression upon sesamin treatment. The therapeutic effect of sesamin in LUAD was measured using a subcutaneous mouse model. Our results indicated that sesamin inhibited the proliferation, survival and migration of LUAD cells (A549 and CL1‑5) in a dose‑dependent manner. Sesamin also enhanced the proapoptotic effects of chemotherapeutic agents such as docetaxel and paclitaxel through the activation of the caspase‑3/poly(ADP‑ribose) polymerase pathway. In addition, sesamin reduced cancer cell migration and anoikis resistance by downregulating the expression of N‑cadherin and inhibiting the phosphoinositide 3‑kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. It also induced the downregulation of programmed death ligand 1 through hsa‑microRNA‑34a‑5p, resulting in the increased cytotoxicity of natural killer cells. This sequence of events consequently interfered with the immune evasion mechanism of LUAD cells. In conclusion, sesamin has a multifaceted effect on the migration, anoikis resistance and antitumor immunity of LUAD cells, indicating its potential as adjunctive therapy.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12440275/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alteration of cardiac energetics and mitochondrial function in doxorubicin‑induced cardiotoxicity: Molecular mechanism and prospective implications (Review).","authors":"Gong Qing, Chao Huang, Jixiang Pei, Bo Peng","doi":"10.3892/ijmm.2025.5624","DOIUrl":"10.3892/ijmm.2025.5624","url":null,"abstract":"<p><p>Doxorubicin (DOX)‑induced cardiotoxicity (DIC) remains a critical challenge in cancer therapy, significantly limiting its use in clinical practice. The underlying mechanisms involve disruptions in cardiac metabolism and mitochondrial dysfunction. The heart relies on mitochondrial oxidative phosphorylation to produce ATP, which is essential for maintaining both contraction and relaxation. DOX disrupts glucose metabolism and fatty acid oxidation, resulting in energy shortages and excessive production of reactive oxygen species (ROS). These ROS contribute to mitochondrial damage, organelle malfunction and eventually cardiomyocyte death. This review describes the pathophysiological aspects of DIC, emphasising the molecular mechanisms underlying mitochondrial dysfunction and metabolic dysregulation in the heart during DIC progression. Additionally, the potential diagnostics, therapeutic interventions and drugs targeting metabolic pathways are summarised, focusing on metabolic modulation, combining non‑pharmacological therapies, such as exercise, fasting and mitochondrial transplantation, and approaches to enhance mitochondrial quality control, offering promising theoretical insights and practical strategies for DIC prevention and management.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425352/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic‑ncRNA crosstalk in atherosclerosis: Mechanisms, disease progression and therapeutic potential (Review).","authors":"Ying Zhu, Zhixin Hu, Jianshuo Liu, Huaqing Duan, Jiqiang Zeng, Xiaosheng Li, Yang Tang, Ziling Song, Zhipeng Wu, Shanrong Zhang, Yuxuan Zhang, Fang Qiu, Chen Lu","doi":"10.3892/ijmm.2025.5621","DOIUrl":"10.3892/ijmm.2025.5621","url":null,"abstract":"<p><p>Atherosclerosis is a chronic and progressive vascular disease involving the gradual accumulation of lipids, cholesterol, cellular debris, and fibrous elements within the arterial wall. This process leads to the thickening and hardening of arteries, resulting in restricted blood flow and reduced oxygen delivery to tissues. Over time, these pathological changes significantly elevate the risk of life‑threatening cardiovascular events, including myocardial infarction and ischemic stroke. Recent studies emphasize the significant role of epigenetic modifications and non‑coding RNAs (ncRNAs) in regulating the progression of atherosclerosis. Histone modifications, DNA methylation, and ncRNAs interact to modulate gene expression, influencing endothelial dysfunction, lipid metabolism, and inflammatory processes. Epigenetic regulators, such as DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), control key vascular genes, while ncRNAs like microRNAs (miRNAs), long non‑coding RNAs (LncRNAs), and circular RNAs (circRNAs) contribute to the modulation of cholesterol efflux and foam cell formation. Understanding the complex interplay between these molecular pathways offers new therapeutic insights for managing atherosclerosis and its complications. The reversible nature of epigenetic changes, alongside ncRNA‑based therapies, holds promising potential for future clinical applications, though challenges such as delivery mechanisms and specificity remain.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12425339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L‑type amino acid transporter 1 in enhancing boron neutron capture therapy: Mechanisms, challenges and future directions (Review).","authors":"Xiaoqing Zheng, Jianji Pan, Donghai Lin, Wei Shao","doi":"10.3892/ijmm.2025.5611","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5611","url":null,"abstract":"<p><p>L‑type amino acid transporter 1 (LAT1) has emerged as a critical molecular target for advancing boron neutron capture therapy (BNCT), a promising treatment that leverages selective boron accumulation and neutron irradiation to eradicate cancer cells. The frequent upregulation of LAT1 in aggressive tumors (such as gliomas and specific subtypes of lung and breast cancer) underpins its essential role as the principal mediator of tumor‑selective boron compound uptake in BNCT. The present review comprehensively examines the structure and function of LAT1, the mechanistic principles of boron transport (including LAT1 mediation) and the key regulatory pathways governing BNCT efficacy. Building on this and given the role of LAT1 in reprogramming tumor metabolism through amino acid transport, advanced metabolomics tools, particularly liquid chromatography‑mass spectrometry and nuclear magnetic resonance, offer a novel approach for clarifying the contribution of LAT1 to BNCT. These techniques hold significant potential to map metabolic profiles altered by LAT1‑mediated boron compound uptake, thereby elucidating downstream biochemical consequences relevant to the therapeutic efficacy and resistance mechanisms. Synthesizing the dual role of LAT1 as both a vulnerability and therapeutic target in BNCT, the present review systematizes key challenges, including the need for selective boron compounds, resistance mechanisms and off‑target effects, while mapping actionable pathways to unlock its potential via refined regulation strategies, next‑generation delivery agents and personalized approaches. By addressing these knowledge gaps, this synthesis provides a foundational framework to harness LAT1‑targeted BNCT, offering potential to advance precision oncology paradigms and improve clinical outcomes for patients with LAT1‑enriched tumors.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373437/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953291","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Expression of Concern] PI3K/Akt signaling pathway‑induced heme oxygenase‑1 upregulation mediates the adaptive cytoprotection of hydrogen peroxide preconditioning against oxidative injury in PC12 cells.","authors":"Liqiu Mo, Chuntao Yang, Mofa Gu, Dongdan Zheng, Lin Lin, Xiuyu Wang, Aiping Lan, Fen Hu, Jianqiang Feng","doi":"10.3892/ijmm.2025.5609","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5609","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, for the cell viability experiments shown in Fig. 2E, the 'Control' image (top row) and the 'ZnPP' image (bottom row) appeared to show an overlapping section of data, such that data which were intended to have shown the results of differently performed experiments appeared to have been derived from the same original source. The authors were contacted by the Editorial Office to offer an explanation for the apparent anomaly in the presentation of the data in this paper, although up to this time, no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 30: 314‑320, 2012; DOI: 10.3892/ijmm.2012.1002].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current status of severe fever with thrombocytopenia syndrome in China (Review).","authors":"Hao Sun, Quanman Hu, Saiwei Lu, Yanyan Yang, Li Zhang, Jinzhao Long, Yuefei Jin, Haiyan Yang, Shuaiyin Chen, Guangcai Duan","doi":"10.3892/ijmm.2025.5610","DOIUrl":"https://doi.org/10.3892/ijmm.2025.5610","url":null,"abstract":"<p><p>Severe fever with thrombocytopenia syndrome (SFTS) is a newly emerging tick‑borne infectious disease caused by the novel Bunyavirus/SFTS virus (SFTSV). The clinical manifestations mainly include fever, thrombocytopenia and multi‑organ dysfunction, with a fatality rate as high as 30%. Since its first report in China in 2009, cases have subsequently emerged in multiple countries across East and Southeast Asia. SFTS demonstrates clear seasonal trends from May to November and tends to cluster geographically, mainly in hilly and mountainous areas. The virus is transmitted through tick bites, animal contact and human‑to‑human transmission. Its genetic diversity and frequent genetic recombination exacerbate public health threats. Pathogenic mechanism studies have shown that SFTSV uses glycoproteins Gn/Gc to mediate host cell invasion. In the early stage, the virus uses its non‑structural protein NSs to inhibit innate immune signal transduction. Massive replication of the virus leads to excessive immune activation, triggering cytokine storms and abnormal platelet activation, and eventually resulting in bleeding and multiple organ failure. The clinical management primarily relies on supportive care, while broad‑spectrum antiviral drugs and neutralizing antibodies remain investigational. Although numerous vaccine candidates have been designed and developed, none have progressed to clinical trials. This review systematically integrates current knowledge spanning virology, epidemiology, pathogenic mechanisms, therapeutic interventions and vaccine development, offering actionable insights for public health strategies and clinical practice.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 5","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}