International journal of molecular medicine最新文献

{"title":"Research progress on mesenchymal stem cell‑derived exosomes in the treatment of osteoporosis induced by knee osteoarthritis (Review).","authors":"Hai-Yan Xue, Xiang-Lin Shen, Zhi-Hua Wang, Hang-Chuan Bi, Hong-Guo Xu, Jie Wu, Ruo-Mei Cui, Ming-Wei Liu","doi":"10.3892/ijmm.2025.5601","DOIUrl":"10.3892/ijmm.2025.5601","url":null,"abstract":"<p><p>Knee osteoarthritis (KOA) and osteoporosis (OP) are closely related, age‑related, degenerative orthopedic conditions. Elderly patients with OP frequently develop concurrent KOA, with high co‑occurrence rates. Studies indicate that OP significantly increases KOA risk and that these conditions mutually exacerbate each other. Anti‑OP therapies show significant efficacy in KOA management, substantially delaying disease progression. Mesenchymal stem cell‑derived exosomes (MSC‑Exos) have significant therapeutic potential for both KOA and OP. These exosomes enhance chondrocyte proliferation, modulate cartilage matrix synthesis and degradation, and suppress synovial inflammation, suggesting a novel therapeutic approach for KOA. However, their OP mechanisms remain unclear but may involve disrupted bone metabolic signaling, amplified inflammation, and dysregulated intercellular communication in the bone microenvironment. The present review summarizes MSC‑Exos research advances in KOA and OP, providing a foundation for future studies and clinical applications.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760059","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":"Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).","authors":"Yuanxia Zou, Jian Dai, Jianchun Li, Min Liu, Run Li, Guiping Li, Junyu Lai, Li Wang","doi":"10.3892/ijmm.2025.5603","DOIUrl":"10.3892/ijmm.2025.5603","url":null,"abstract":"<p><p>The progression from acute kidney injury (AKI) to chronic kidney disease (CKD) has become a focal point of investigation, with the TGF‑β/Smad signaling pathway emerging as a key mediator in this process. The present review assesses how TGF‑β/Smad contributes to renal fibrosis and the subsequent deterioration of kidney function following AKI. Drawing on recent experimental and clinical findings, this study explores how pathway activation promotes tubular cell injury, inflammation and interstitial fibrosis. By examining these molecular and cellular events, this study offers fresh insights into the complex mechanisms that underlie the AKI‑CKD transition and highlights potential therapeutic strategies aimed at interrupting or slowing disease progression.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760060","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":"Bmi1 regulates neural differentiation of mesenchymal stem cells through the Wnt3a‑RhoA signaling pathway to repair ischemic brain injury in rats.","authors":"Kunling Chen, Hongjie Zhou, Jie Zhang, Yiwei Zhang, Xiaobing Dou, Qin Yu, Liping Zhou","doi":"10.3892/ijmm.2025.5596","DOIUrl":"10.3892/ijmm.2025.5596","url":null,"abstract":"<p><p>Ischemic brain injury (IBI) is characterized by high morbidity, disability and mortality rates; however, it lacks effective clinical treatments. Mesenchymal stem cells (MSCs), as pluripotent stem cells with self‑renewal capacity and multilineage differentiation potential, have emerged as a promising therapeutic strategy for neurological disorders. In the present study, <i>in vitro</i> experiments were performed using the Wnt signaling agonist Wnt3a and the B lymphoma Mo‑MLV insertion region 1 homolog (Bmi1) small molecule inhibitor PTC209 to treat MSCs, and the roles and regulatory mechanisms of the Bmi1 and Wnt3a‑RhoA signaling pathways on the neural differentiation of MSCs were explored by MTT assay, immunofluorescence analysis and western blotting. <i>In vivo</i> experiments were also performed by establishing a rat model of middle cerebral artery occlusion (MCAO), transplanting different MSCs into the rat brain tissues after <i>in vitro</i> labeling, and comparing ischemic brain damage in each group of rats by Neurological Severity Score scoring, grasp assay, triphenyltetrazolium chloride staining, hematoxylin and eosin staining, and assessing neurological recovery via immunofluorescence and western blot analysis. The <i>in vivo</i> study aimed to assess the roles of the Bmi1 and Wnt3a‑RhoA signaling pathways in brain injury repair in MCAO rats and the mechanism. Specifically, recombinant Wnt3a cytokine was administered to upregulate the Wnt3a‑RhoA pathway, whereas the small‑molecule inhibitor PTC209 was utilized to suppress Bmi1 expression. The findings suggested that Bmi1 modulates the neural differentiation of MSCs through its regulatory effects on Wnt3a and RhoA expression, thereby influencing the reparative potential of MSCs in ischemic brain tissue. These findings highlight the therapeutic relevance of targeting Wnt3a‑RhoA activation and Bmi1 inhibition in MSC‑based interventions for IBI.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12339166/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144707442","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":"Protective effect of exercise on metabolic dysfunction‑associated fatty liver disease: Potential epigenetic mechanisms (Review).","authors":"Yanhua Zhang, Yuqin Wei, Huan Liu, Yanju Guo","doi":"10.3892/ijmm.2025.5587","DOIUrl":"10.3892/ijmm.2025.5587","url":null,"abstract":"<p><p>Metabolic dysfunction‑associated fatty liver disease (MAFLD) is the most prevalent cause of chronic liver disease worldwide and poses a major health burden that is closely linked to obesity, insulin resistance and type 2 diabetes. While extensive research has elucidated key molecular drivers, no pharmacological therapies have been approved. Emerging evidence highlights the transformative role of physical exercise as a potent nonpharmacological intervention capable of inducing durable metabolic improvements. Epigenetic remodeling, which encompasses DNA methylation, histone modifications and non‑coding RNA regulation, has been increasingly recognized as a key mechanism driving these long‑lasting effects. Aberrant epigenetic modifications disrupt hepatic lipid metabolism, mitochondrial function, autophagy, inflammation and fibrosis progression, thereby driving MAFLD pathogenesis. The present review comprehensively covers the current knowledge on epigenetic mechanisms implicated in MAFLD and systematically assesses how distinct exercise modalities reshape these epigenetic landscapes to restore hepatic metabolic homeostasis. Understanding the epigenetic underpinnings of exercise‑induced hepatic protection offers a promising avenue for advancing personalized interventions and novel therapeutics for MAFLD.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 4","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12289129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667611","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":"MEIS1‑regulated miR‑488‑3p suppresses the malignant progression of laryngeal squamous cell carcinoma by targeting ACVR1C.","authors":"Chunming Zhang, Wenjing Hao, Xinfang Wang, Huina Guo, Long He, Jiao Yang, Ying Wang, Xiwang Zheng, Zhongxun Li, Qi Han, Liqi Wen, Hongliang Liu","doi":"10.3892/ijmm.2025.5583","DOIUrl":"10.3892/ijmm.2025.5583","url":null,"abstract":"<p><p>Laryngeal squamous cell carcinoma (LSCC) is a common malignant tumor originating from the mucosal epithelium of the larynx. MicroRNA (miR)‑488‑3p has non‑negligible multifaceted roles in some types of cancer; however, its association with LSCC has not yet been reported. Our prior RNA sequencing data indicated that miR‑488‑3p expression is downregulated in LSCC tissue, yet the detailed function and regulatory mechanism of miR‑488‑3p in LSCC remain unknown. In the present study, quantitative PCR analysis corroborated the significant downregulation of miR‑488‑3p in LSCC tumor tissues, with this downregulation being strongly associated with malignant progression in LSCC. Furthermore, overexpression of miR‑488‑3p suppressed LSCC cell proliferation, colony formation, migration, invasion, xenograft tumor growth and epithelial‑mesenchymal transition. Mechanistically, miR‑488‑3p directly interacted with the 3' untranslated region of activin A receptor type 1C (ACVR1C) and downregulated ACVR1C expression. Functional experiments revealed that miR‑488‑3p suppressed the malignant phenotypes of LSCC via ACVR1C. Additionally, bioinformatics analysis coupled with chromatin immunoprecipitation assay revealed that myeloid ecotropic viral integration site 1 (MEIS1) promoted the expression of miR‑488‑3p transcriptionally by directly binding its promoter region. Collectively, the results demonstrated that miR‑488‑3p acts as a tumor suppressor molecule in LSCC, and a role was established for the MEIS1/miR‑488‑3p/ACVR1C axis in regulating LSCC progression, thus providing novel potential biomarkers and targets for patients with LSCC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.8,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667603","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":"RBM8A promotes gastric cancer progression by binding with UPF3B to induce BBC3 mRNA degradation.","authors":"Hang Peng, Long Zhang, Fang Li, Xintao Jing, Jing Zhou, Li Cao, Cuixiang Xu, Jianhua Wang, Chen Huang","doi":"10.3892/ijmm.2025.5572","DOIUrl":"10.3892/ijmm.2025.5572","url":null,"abstract":"<p><p> RNA metabolism is an important post‑transcriptional regulatory mode in organisms, and its process is cooperatively regulated by a variety of RNA‑binding proteins. RNA binding motif protein 8A (RBM8A), a regulator of mRNA stability that is implicated in cancer progression, serves an important role in processes such as RNA splicing, transport, translation and decay. However, to the best of our knowledge, its role in the occurrence and development of gastric cancer (GC), as well as its biological functions and molecular mechanisms remain unclear. In the present study, RBM8A expression was on average 1.4‑fold higher (P<0.05), with a maximum log2 fold change of 1.4 (2.6‑fold increase), in GC tissues compared with adjacent normal tissues, as determined by multiplex immunohistochemical analysis of tissue microarrays. <i>In vitro</i>, transfection of RBM8A small interfering RNAs significantly suppressed the proliferation of AGS and HGC27 cells and enhanced apoptosis. Specifically, annexin V‑positive AGS cells exhibited a 2.9‑fold increase with siRBM8A‑1 transfection and a 1.9‑fold increase with siRBM8A‑2 transfection, while annexin V‑positive HGC27 cells exhibited a 2.3‑fold increase with siRBM8A‑1 transfection and a 1.8‑fold increase with siRBM8A‑2 transfection (P<0.05). Using MKN45 cell lines and subcutaneous xenograft models, the present study revealed that RBM8A knockdown reduced subcutaneous tumor growth in nude mice by 51.5% in terms of volume and 62.4% in terms of weight (P<0.05). In terms of the mechanism, integrated mRNA‑sequencing (seq) and RNA immunoprecipitation (RIP)‑seq identified BCL2 binding component 3 (BBC3), a well‑characterized pro‑apoptotic gene, as a direct target of RBM8A. Further results of RIP‑quantitative PCR, fluorescence <i>in situ</i> hybridization‑immunofluorescence and RNA pulldown indicated the direct interaction between RBM8A and BBC3 mRNA. Actinomycin D assays demonstrated that RBM8A promoted BBC3 mRNA degradation. Subsequently, the co‑immunoprecipitation assay showed that RBM8A interacted with UPF3B to jointly regulate the stability of BBC3 mRNA. In conclusion, RBM8A inhibited apoptosis and promoted GC progression by interacting with UPF3B, leading to degradation of the pro‑apoptotic gene BBC3 mRNA. These findings highlighted that interfering with RBM8A expression, or disrupting the interactions between RBM8A and BBC3 mRNA or between RBM8A and UPF3B could serve as potential therapeutic strategies for GC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236746/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560128","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":"Benzo[a]pyrene aggravated ovalbumin‑induced epithelial tight junction disruption via ROS driven‑NLRP3/Caspase‑1 signaling pathway in asthmatic mice.","authors":"Yanqiu Xu, Yanming Feng, Ling Wang, Xin Xu, Li Xu, Bohan Wang","doi":"10.3892/ijmm.2025.5573","DOIUrl":"10.3892/ijmm.2025.5573","url":null,"abstract":"<p><p>Air pollutants contribute to the occurrence and development of asthma by impairing the airway epithelial barrier. However, underlying molecular mechanisms remain unknown. The present study investigated whether co‑exposure to the air pollutant benzo[a]pyrene (BaP) and ovalbumin (OVA) enhanced OVA‑induced epithelial tight junction disruption and explored the potential mechanisms involved. Asthma mouse and airway epithelial cell models were established and exposed to BaP. Lung pathology, immunoglobulin E (IgE), tight junction proteins zonula occludens‑1 (ZO‑1) and occludin, reactive oxygen species (ROS), NOD‑like receptor protein 3 (NLRP3), apoptosis‑associated speck‑like protein containing a CARD, caspase‑1, interleukin (IL)‑18 and IL‑1β were assessed by hematoxylin‑eosin staining, enzyme‑linked immunosorbent assay, western blotting, immunohistochemistry and immunofluorescence. Inhibitors of ROS and NLRP3 were used to assess their effect on ZO‑1 and occludin and downstream signaling pathways to clarify BaP‑induced damage. Lung tissue damage was exacerbated by BaP, the IgE level increased and the ZO‑1 and occludin expression reduced in both models, thereby disrupting airway epithelial tight junctions. Additionally, BaP increased ROS levels and activated the NLRP3/caspase‑1 signaling pathway. However, reducing ROS and NLRP3 restored the ZO‑1 and occludin expression and improved epithelial integrity. Airway tight junction disruption was promoted by BaP by activating the ROS‑driven NLRP3/caspase‑1 signaling pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560123","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":"Blood‑brain barrier dysfunction in epilepsy: Mechanisms, therapeutic strategies and future orientation (Review).","authors":"Na Huang, Yawen Huang, Zhenyuan Deng, Shuya Qi, Wei Zhang, Yuanyuan Liu, Guohe Tan","doi":"10.3892/ijmm.2025.5577","DOIUrl":"10.3892/ijmm.2025.5577","url":null,"abstract":"<p><p>The blood‑brain barrier (BBB) is a crucial structure for maintaining homeostasis within the central nervous system, and its integrity plays a pivotal role in the onset and progression of epilepsy. Epileptic seizures can disrupt the molecular architecture of the BBB, including the loss of tight junction proteins, activation of matrix metalloproteinases and dysfunction of supporting cells. Various pathological changes, such as transmembrane transport disorders, upregulation of platelet‑derived growth factor receptor β and vascular endothelial growth factor signalling pathways, and activation of astrocytes and microglia, accompany these alterations. These modifications exacerbate the entry of toxic molecules (such as albumin) into the brain parenchyma, triggering neuroinflammation and neuronal damage, thereby establishing a vicious cycle of epilepsy, BBB disruption and recurrent epilepsy. Consequently, repairing or protecting the BBB is a novel strategy for controlling epileptic seizures and treating drug‑resistant epilepsy. Consequently, compared with current treatment approaches that primarily focus on suppressing neuronal excitability, repairing or protecting the BBB is a novel strategy for controlling epileptic seizures and treating drug‑resistant epilepsy. Drugs such as botulinum, levetiracetam and angiotensin receptor blockers show the potential for BBB protection. The development of nanomaterials can enhance drug concentrations in affected areas, thereby offering new avenues for refractory epilepsy. The present study systematically reviews the critical role of the BBB in the pathogenesis of epilepsy, untangles the complex association between BBB dysfunction and the course of the disease, aims to deepen our understanding of the molecular mechanisms underlying BBB damage, and explores new approaches for epilepsy prevention and treatment from a BBB perspective. This review provides a theoretical foundation and research direction for the development of diagnostic and treatment strategies that are safer and more effective than current standard therapies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560124","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 anti‑VEGF on peripapillary retinal nerve fiber layer and papillary/peripapillary blood circulation in retinopathies (Review).","authors":"Hongwei Wang, Renfeng Ding, Wenya Jiang, Siyi Li, Yijuan Wu, Junfeng Mao, Yanan Chen, Peng Sun, Mengqi Shi","doi":"10.3892/ijmm.2025.5574","DOIUrl":"10.3892/ijmm.2025.5574","url":null,"abstract":"<p><p>Vascular endothelial growth factor (VEGF) is an endothelial cell‑specific angiogenic factor. VEGF is involved in vasodilatation, nerve protection and retinal development and maturation. Over‑expression of VEGF is closely associated with retinopathies, such as retinal vein occlusion, diabetic retinopathy, age‑related macular degeneration and diabetic macular edema. Intravitreal injections of anti‑VEGFs are widely used in the treatment of retinopathies to reduce the angiogenesis and the macular edema. Hypothetically, repeated anti‑VEGF injections for retinopathies should interfere with the neuroprotective function of VEGF and might induce the vasoconstriction with a subsequent decrease in the ocular perfusion. These two could affect the optic nerve. The peripapillary retinal nerve fiber layer (p‑RNFL) thinning and the decreased papillary/peripapillary blood circulation can show the optic nerve damage earlier. In the present review, the effects of anti‑VEGFs on p‑RNFL and papillary/peripapillary blood circulation in retinopathies were comprehensively summarized and analyzed to explore whether the anti‑VEGFs cause damages to the optic nerve. The present review provided a detailed evaluation and analysis of the changes in p‑RNFL thickness, papillary/peripapillary blood circulation and intraocular pressure and the correlations between these changes with the number and type of anti‑VEGFs in 3,078 affected eyes and 520 fellow eyes with retinopathies. The present review sought to establish a foundation for the intravitreal administration of anti‑VEGFs and efficacy monitoring of the possible side effects on the optic nerve.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560125","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":"Histone deacetylase 6: A new player in oxidative stress‑associated disorders and cancers (Review).","authors":"Fei Qu, Qingqing Zhao, Yi Jin","doi":"10.3892/ijmm.2025.5578","DOIUrl":"10.3892/ijmm.2025.5578","url":null,"abstract":"<p><p>Histone deacetylase 6 (HDAC6), a distinctive member of the histone deacetylase family, plays a crucial role in regulating the cellular response to oxidative stress. Unlike other HDACs, HDAC6 primarily deacetylates non‑histone proteins, influencing various cellular functions critical to the pathogenesis of numerous oxidative stress‑related diseases. This review summarizes the latest research on how HDAC6 affects oxidative stress pathways and its impact on diseases such as neurodegeneration, cancer and cardiovascular disorders. Additionally, the therapeutic potential of targeting HDAC6, as evidenced by preclinical trials, was discussed, suggesting that HDAC6 inhibitors can ameliorate symptoms and alter disease progression in numerous disease models. By elucidating the multifaceted roles of HDAC6 in oxidative stress and disease, the review aims to underscore its potential as a therapeutic target. This review enhances the understanding of HDAC6 and presents new opportunities for innovative treatment approaches that can address oxidative stress‑related illnesses.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12270379/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608307","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}