International journal of molecular medicine最新文献

{"title":"Monocytes in pneumonia: Functional plasticity and innate memory (Review).","authors":"Run-Ze Li, Zhi-Han Xie, Li Chen, Yun-Xiao Shang, Fei Wang, Wan-Jie Huang, Qi Cheng","doi":"10.3892/ijmm.2026.5986","DOIUrl":"10.3892/ijmm.2026.5986","url":null,"abstract":"<p><p>Pneumonia remains one of the most prevalent and deadly respiratory diseases worldwide, imposing substantial clinical and socioeconomic burdens. Monocytes (Mos) and their progeny are key components of the innate immune system and perform highly context‑dependent roles. The present review summarizes recent advances in understanding Mo biology in pneumonia and discusses current concepts of their functional plasticity. The review first summarizes the developmental origins, phenotypic heterogeneity and functions of circulating Mo subsets, followed by an overview of their recruitment, activation and differentiation in the steady‑state and infected lung. Next, the dual, and at times opposing, roles of Mos and their progeny in pneumonia are examined, including contributions to pathogen clearance and microbial immune evasion, the initiation and resolution of inflammation, and tissue repair vs. fibrotic remodeling. Finally, the review highlights emerging evidence showing that pneumonia can induce durable innate immune memory in Mos, their progenitors and the alveolar macrophage compartment. This reprogramming may reshape subsequent pulmonary and systemic immune responses, with important implications for susceptibility to reinfection, chronic lung dysfunction and host resilience. A deeper understanding of Mo plasticity and innate memory may open new avenues for biomarker discovery and host‑directed therapeutic strategies for pneumonia.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592807/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989935","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] PAT protein mRNA expression in primary rat hepatocytes: Effects of exposure to fatty acids.","authors":"Elena Grasselli, Adriana Voci, Carlo Pesce, Laura Canesi, Emilia Fugassa, Gabriella Gallo, Laura Vergani","doi":"10.3892/ijmm.2026.5995","DOIUrl":"10.3892/ijmm.2026.5995","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the ORO‑stained hepatocyte images shown in Fig. 3B on p. 510, the 'C 12h' and 'C 36h' data panels were strikingly similar in appearance (albeit one panel was sized slightly differently relative to the other), suggesting that the data in this figure had been assembled incorrectly. The authors have been contacted by the Editorial Office to offer an explanation for the apparent data duplication in Fig. 3B in this paper, and we are awaiting their response. Due to the fact that we have 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 25: 505‑512, 2010; DOI: 10.3892/ijmm_00000370].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13614615/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038481","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":"miR‑222‑3p inhibits diabetic skin wound healing by targeting APLN.","authors":"Ruyan Jie, Ying Tang, Tingting Wu, Chenfan Zhang, Man Song, Xiaotong Zhao, Mingwei Chen","doi":"10.3892/ijmm.2026.6002","DOIUrl":"10.3892/ijmm.2026.6002","url":null,"abstract":"<p><p>Diabetic foot ulcer (DFU) is a severe complication of diabetes, characterized by chronic, difficult‑to‑heal foot wounds. It has been hypothesized that miR‑222‑3p may influence wound healing via the regulation of angiogenesis. To elucidate the underlying mechanism, experimental investigations were conducted <i>in vitro</i> using human dermal microvascular endothelial cells (HMEC‑1) and <i>in vivo</i> in a mouse model of streptozotocin‑induced diabetes. Methylglyoxal (MGO), a glycolytic intermediate, is known to contribute to diabetic vascular complications. The results demonstrated that MGO‑treated HMEC‑1 cells exhibited an increased expression of miR‑222‑3p and impaired microvascular endothelial cell function. The overexpression of miR‑222‑3p in MGO‑treated HMEC‑1 cells further suppressed cell proliferation, migration and tube formation, while it enhanced apoptosis. Moreover, the upregulation of miR‑222‑3p reduced the expression of apelin (APLN), and dual‑luciferase reporter assays confirmed APLN as a direct downstream target of miR‑222‑3p. The silencing of APLN markedly impaired HMEC‑1 cell function. Notably, both the exogenous supplementation with Apelin‑13 and the overexpression of APLN significantly reversed endothelial dysfunction caused by the upregulation of miR‑222‑3p. <i>In vivo</i>, in both normal and diabetic mice, the elevated expression of miR‑222‑3p in skin wounds reduced APLN levels in the peri‑wound tissue and impaired wound healing. However, the overexpression of APLN or the inhibition of miR‑222‑3p with an antagomiR reversed this impairment. Collectively, these results suggest that miR‑222‑3p impairs microvascular endothelial cell function by targeting APLN, thereby contributing to delayed wound healing in diabetic skin.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637565/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109237","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":"[Retracted] Silencing of decoy receptor 3 (DcR3) expression by siRNA in pancreatic carcinoma cells induces Fas ligand‑mediated apoptosis <i>in vitro</i> and <i>in vivo</i>.","authors":"Jian Zhou, Shiduo Song, Songbin He, Zhenxin Wang, Bing Zhang, Dechun Li, Dongming Zhu","doi":"10.3892/ijmm.2026.5971","DOIUrl":"10.3892/ijmm.2026.5971","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that, regarding the EdU assay experiments shown in Fig. 6 on p. 657, discrete areas of the cells appeared to overlap in different data panels, which were intended to show differently performed experiments in two distinct cell lines (the SW1990 and Panc‑1 cell lines), albeit the areas were inverted in the case of the 'LV‑RNAi' data panels. Moreover, within these areas of overlapping cells, certain of the cells were uniquely found to be coloured differently in the associated data panels. In addition, in Fig. 9 on p. 658, the bands shown for the caspase‑3 and caspase‑3 experiments with the SW1990 cell line looked remarkably similar, suggesting that the data in this figure may also have been assembled incorrectly. After having conducted an internal investigation of the data in this paper, the Editor of <i>International Journal of Molecular Medicine</i> has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 32: 653‑660, 2013; DOI: 10.3892/ijmm.2013.1437].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891204","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":"Advances in sirtuin research in lung diseases (Review).","authors":"Shuangyun Xi, Weijun Chen, Xiuli Li, Yudan Wang, Yong Ke","doi":"10.3892/ijmm.2026.5967","DOIUrl":"10.3892/ijmm.2026.5967","url":null,"abstract":"<p><p>Sirtuins, which comprise a family of NAD+-dependent deacetylases, have emerged as critical regulators in the pathogenesis of pulmonary diseases because of their pleiotropic roles in oxidative stress, metabolic homeostasis and inflammation. Growing evidence indicates that sirtuins modulate key cellular processes, including mitochondrial function, cell survival and death pathways, via protein deacetylation, thereby influencing disease progression in chronic obstructive pulmonary disease, pulmonary fibrosis and lung cancer. Notably, dysregulated sirtuin expression and activity are implicated in various lung pathologies, highlighting their dual potential as diagnostic biomarkers and therapeutic targets. The present review synthesized recent advances in sirtuin research, focusing on molecular mechanisms and translational applications, to provide a foundation for developing novel strategies for lung disease prevention and treatment. A comprehensive literature review of the relationship between sirtuins and lung‑related diseases was conducted. Literature published in PubMed and Web of Science up to May 2025 was searched using the keywords 'sirtuin,' 'SIRTs,' 'lung disease,' and 'pulmonary disease.'</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840007","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":"Spatial multi‑omics identifies an SPP1+ macrophage‑driven anti‑apoptotic niche in osteoarthritis synovium via the SPP1‑CD44 axis.","authors":"Han Gong, Hao Shen, Feng Zhang, Wei Wang, Sheng Zhou, Lei Wang, Yu Sun","doi":"10.3892/ijmm.2026.6005","DOIUrl":"10.3892/ijmm.2026.6005","url":null,"abstract":"<p><p>Osteoarthritis (OA) progression is driven by chronic synovitis. However, the spatially organized macrophage subsets that sustain unresolved inflammation through evasion of apoptosis remain poorly characterized. The present study investigated the functional subsets and spatial niches of synovial macrophages that regulate apoptotic pathways in OA pathogenesis. Spatial transcriptomics, single‑cell RNA sequencing and <i>in vitro</i> apoptotic models were integrated to characterize macrophage interactions in the OA synovium. The anti‑apoptotic role of SPP1⁺ macrophages was evaluated using adeno‑associated virus‑mediated macrophage‑targeted SPP1 knockdown and CCL3 neutralization in a mouse OA model. In addition, an <i>in silico</i> virtual knockout model was employed to delineate SPP1‑mediated apoptotic regulatory networks and prioritize candidate compounds for future validation. Spatial multi‑omics revealed a TGF‑β‑enriched niche in which SPP1+ macrophages expand adjacent to senescent synovial fibroblasts. Distinct from their reported pro‑fibrotic roles, SPP1⁺ macrophages directly suppressed apoptosis of inflammatory macrophages via the SPP1‑CD44 signaling axis, while recruiting additional myeloid cells through CCL3 secretion. <i>In vivo</i>, targeting SPP1 or neutralizing CCL3 effectively restored macrophage apoptosis, attenuated synovitis and cartilage degeneration. <i>In silico</i> myeloid specific SPP1 knockout delineated apoptotic pathway perturbations. In conclusion, TGF‑β‑induced SPP1⁺ macrophages establish an anti‑apoptotic inflammatory niche in OA synovium by directly inhibiting the apoptosis of inflammatory macrophages via SPP1 signaling and promoting myeloid recruitment. This spatially defined anti‑apoptotic circuit provides critical insight into persistent synovitis.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13637569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149109268","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":"ILC3s as central regulators of mucosal homeostasis and disease pathogenesis (Review).","authors":"Jingwen Zhang, Lili Bao, Jiaxi Li, Xia Li, Lu Qiao, Jiaxian Cui, Xiaoxia He, Mingyu Zhang, Jingkun Lu, Xuan Zhang, Jing Dong, Gesi Tao, Yaoqing Feng, Yun Peng Tian, Pengwei Zhao, Ya Tuo","doi":"10.3892/ijmm.2026.5991","DOIUrl":"10.3892/ijmm.2026.5991","url":null,"abstract":"<p><p>Type 3 innate lymphoid cells (ILC3s) constitute key components of mucosal innate immunity and serve key roles in maintaining mucosal barrier homeostasis and regulating inflammatory responses. The present review summarizes the biological characteristics and regulatory mechanisms of ILC3s, while discussing their interactions with the gut microbiota and pathological functions in mucosa‑associated disorders. Derived from bone marrow‑resident common lymphoid progenitors, ILC3s differentiate under the transcriptional control of retinoid‑related orphan receptor γ‑t into distinct functional subsets, including natural cytotoxicity receptor (NCR)+ ILC3s, NCR‑ ILC3s and lymphoid tissue inducer cells. ILC3s maintain epithelial barrier integrity, enhance antimicrobial defense and support lymphoid tissue development through the production of effector molecules such as IL‑22, IL‑17 and granulocyte‑macrophage colony‑stimulating factor. These subsets can undergo phenotypic conversion in response to microenvironmental signals. ILC3 activity is tightly regulated by transcription factors, metabolic pathways, neuroimmune interactions and the circadian clock system. In addition, ILC3s establish bidirectional interactions with the gut microbiota: Microbial metabolites regulate ILC3 activity, whereas ILC3s influence microbial composition through IL‑22‑dependent antimicrobial peptide production and IgA responses. Depending on subset composition, local cytokine networks and tissue microenvironment, ILC3s may exert either pathogenic or protective effects in a number of diseases. Future investigations should aim to further elucidate the molecular mechanisms underlying ILC3 subset plasticity, tissue‑specific interaction networks and clinically translatable strategies for targeted intervention. Building upon these findings, the present review proposes a spatiotemporal‑quantitative framework and three regulatory axes that may account for disease‑specific variations in ILC3 responses, providing a basis for understanding distinct ILC3 functions and developing targeted therapeutic strategies. Systematic investigation of the regulatory principles governing ILC3 biology will not only deepen the understanding of innate immune homeostasis but also provide potential targets and strategies for precision immunotherapy in diseases such as inflammatory bowel disease and colorectal cancer.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13600334/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989863","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":"Deciphering the function and mechanism of extracorporeal shock wave therapy in knee osteoarthritis (Review).","authors":"Yixuan Chen, Siqi Song, Yuchen Zhu, Shiqi Wang, Jieyuan Hu, Chenxu Liu, Yuchen Cai, Yushi Hu","doi":"10.3892/ijmm.2026.5980","DOIUrl":"10.3892/ijmm.2026.5980","url":null,"abstract":"<p><p>Knee osteoarthritis (KOA) is a chronic, disabling disease with multiple etiologies and a complex pathophysiology. Conservative treatment is the cornerstone of KOA management, and when it proves insufficient, extracorporeal shock wave therapy (ESWT) has emerged as a practical non‑invasive alternative. The present narrative review systematically summarizes current preclinical and clinical evidence on ESWT for KOA through a structured literature search, aiming to integrate its therapeutic effects and identify knowledge gaps. Accumulating evidence indicates that ESWT can slow KOA progression through multiple biological pathways, encompassing anti‑inflammatory, anti‑apoptotic, pro‑proliferative and cartilage‑protective effects, while also relieving pain and improving function clinically. Summarizing the available data, this review finds that ESWT exhibits a favorable safety profile for articular tissues and disease‑modifying potential in preclinical models, although treatment outcomes depend critically on energy flux density and protocol selection. In human studies, the current evidence primarily supports symptomatic relief, including pain reduction and functional improvement; high‑quality trials with structural endpoints to verify cartilage regeneration or joint space preservation remain scarce. Given its non‑invasive nature, safety and growing clinical support, ESWT merits consideration as an adjunctive therapy. However, heterogeneity in treatment parameters and limited long‑term data preclude standardized guidelines. Despite these limitations, ESWT remains a promising adjunctive therapy for patients who are unresponsive to conventional conservative treatments. Future research should prioritize parameter optimization, extended follow‑up and translational studies to bridge the gap between preclinical structural findings and clinical application. Addressing these gaps will strengthen the therapeutic role and scientific foundation of ESWT.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13592809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891259","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":"[Corrigendum] Tumor‑targeting novel manganese complex induces ROS‑mediated apoptotic and autophagic cancer cell death.","authors":"Jia Liu, Wenjie Guo, Jing Li, Xiang Li, Ji Geng, Qiuyun Chen, Jing Gao","doi":"10.3892/ijmm.2026.5968","DOIUrl":"10.3892/ijmm.2026.5968","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that the COX IV western blot data shown in Fig. 3D on p. 611 were strikingly similar to blots that appeared in another article by the same research group that was published in the journal <i>Molecular Medicine Reports</i>. In addition, it was noted that a section of the fluorescence microscopic data shown in Fig. 4A (in the \"Adpa‑Mn 20 μM + 3‑MA\" data panel) bore a strong resemblance to the data shown in Fig. 5A for the \"Adpa‑Mn 20 μM\" experiment. Thirdly, concerns were raised regarding the tumour images shown in Fig. 6A. Certain of the tumours appeared rather large, although a corresponding scale alongside the tumours was not shown in the figure; in addition, the tumour weights reported in Fig. 6B appeared not to be commensurate with the apparent sizes of the tumours, and Fig. 6B showed quantification of the data for three different Adpa‑Mn treatment groups (1 mg/kg, 5 mg/kg and 10 mg/kg), whereas only tumours from the 10 mg/kg group were portrayed in Fig. 6A. Upon re‑examining the raw data belonging to these figures, due to oversights that were made during the final assembly and handling of a large volume of experimental data, the authors realize that some errors were inadvertently made in assembling the data in various of the figures. In Fig. 3, the western blot band for the COX IV loading control was misused, and an incorrect band was included in this figure. In Figs. 4 and 5, certain fluorescence microscopy images were misplaced during the final preparation, leading to the incorrect placement of the data panel in Fig. 4A. Finally, in Fig. 6A, the tumour images for the 1 mg/kg and 5 mg/kg treatment groups had not originally been included, and a scale bar was omitted from Fig. 6A. Concerning the animal experiments, the Editor permitted the authors to repeat the <i>in vivo</i> experiments under rigorous conditions, and in the new version of Fig. 6, a complete set of tumour photographs for all groups has been provided, now including a scale bar. The revised versions of Fig. 3 (showing the correct data for the COX IV western blots in Fig. 3D) and Fig. 4 (showing the correct data for the \"Adpa‑Mn 20 μM + 3‑MA\" panel in Fig. 4A), and the new version of Fig. 6, are shown on the subsequent pages. Note that the errors made during the assembly of these figures did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 35: 607‑616, 2015; DOI: 10.3892/ijmm.2015.2073].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148839907","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":"Research progress on lysine acetylation (Review).","authors":"Minghui Zhang, Yuqi Zhang, Haoxin Yin, Junyuan Yan, Yingling Dong, Xin Zhao, Tianyi Cui, Bin Lv, Xiumei Gao","doi":"10.3892/ijmm.2026.5976","DOIUrl":"10.3892/ijmm.2026.5976","url":null,"abstract":"<p><p>Lysine acetylation is recognized as a critical and reversible post‑translational modification that is essential for numerous cellular functions and biological processes. The dynamic interplay between lysine acetylation and deacetylation to regulates a wide spectrum of processes, including histone modification, gene expression, cell cycle progression, DNA repair and signal transduction. Emerging evidence has demonstrated that the dysregulation of lysine acetylation is strongly associated with multiple diseases, including cancer, cardiovascular diseases, chronic inflammatory diseases and neurological diseases. These alterations can modify gene expression and disrupt cellular homeostasis. The present review aimed to highlight the biological functions of lysine acetyltransferases and lysine deacetylases, their contributions to disease pathogenesis, and the interplay the crosstalk of lysine acetylation with other post‑translational modifications. Drawing on the latest research findings, the therapeutic potential of targeting acetylation pathways is discussed, with the aim of providing new insight into the development of innovative treatment strategies and clinical applications.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"58 5","pages":""},"PeriodicalIF":8.5,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13553044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891497","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}