International journal of molecular medicine最新文献_第5页

Research progress on lysine acetylation (Review). 赖氨酸乙酰化研究进展（综述）

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/ijmm.2026.5976

Minghui Zhang, Yuqi Zhang, Haoxin Yin, Junyuan Yan, Yingling Dong, Xin Zhao, Tianyi Cui, Bin Lv, Xiumei Gao

{"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":"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.","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}

引用次数: 0

Reprogramming of cell death in gastric cancer: From molecular mechanisms to therapeutic potential (Review). 胃癌细胞死亡的重编程：从分子机制到治疗潜力（综述）

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-25 DOI: 10.3892/ijmm.2026.5999

Mengru Liu, Zhujun Wu, Qiao Chen, Weiguo Ni, Ying Chen, Yixin Zhu, Yu Chen, Haifeng Ma, Yan Lin

{"title":"Reprogramming of cell death in gastric cancer: From molecular mechanisms to therapeutic potential (Review).","authors":"Mengru Liu, Zhujun Wu, Qiao Chen, Weiguo Ni, Ying Chen, Yixin Zhu, Yu Chen, Haifeng Ma, Yan Lin","doi":"10.3892/ijmm.2026.5999","DOIUrl":"10.3892/ijmm.2026.5999","url":null,"abstract":"Malignant progression and limited therapeutic response in gastric cancer (GC) cannot be explained solely by increased proliferation or oncogenic alterations. Instead, they reflect how tumor cells regulate their death threshold under sustained damage, metabolic stress and immune pressure. Evidence indicates that GC cells largely retain the capacity for cell death but reduce its effective execution by attenuating signal propagation, weakening key execution steps and altering microenvironmental interactions. As a result, cellular stress persists without effective clearance, promoting survival, resistance and metastasis. The present review synthesized current evidence on the mechanisms and interplay of cell death in GC, with emphasis on their relationships with the tumor microenvironment, host factors and therapeutic stress. It further evaluated their implications for resistance, patient stratification and therapeutic intervention. Reframing GC through the lens of cell death regulation provides a more coherent basis for understanding its biological heterogeneity and for improving therapeutic strategies.","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/PMC13637564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038460","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}

引用次数: 0

Tumor‑immune spatiotemporal co‑evolution: A new paradigm for understanding and overcoming therapy resistance in metastatic castration‑resistant prostate cancer (Review). 肿瘤免疫时空协同进化：理解和克服转移性去势抵抗性前列腺癌治疗耐药性的新范式（综述）。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-25 DOI: 10.3892/ijmm.2026.5997

Li Yan, Xiaoke Sun, Pengxiao Su

{"title":"Tumor‑immune spatiotemporal co‑evolution: A new paradigm for understanding and overcoming therapy resistance in metastatic castration‑resistant prostate cancer (Review).","authors":"Li Yan, Xiaoke Sun, Pengxiao Su","doi":"10.3892/ijmm.2026.5997","DOIUrl":"10.3892/ijmm.2026.5997","url":null,"abstract":"Metastatic castration‑resistant prostate cancer (mCRPC) remains an incurable disease characterized by relentless progression and universal resistance to standard therapies. The limited efficacy of immunotherapies in this malignancy reflects an immunosuppressive tumor microenvironment orchestrated by regulatory T cells, myeloid‑derived suppressor cells, tumor‑associated macrophages and cancer‑associated fibroblasts, along with androgen receptor signaling, metabolic reprogramming and spatially organized immune exclusion zones. The present review synthesized emerging evidence from single‑cell and spatial transcriptomics to propose a spatiotemporal coevolution paradigm, wherein resistance emerges not through linear genetic selection alone but through dynamic, reciprocal interactions among tumor cells, stromal components and immune populations across both temporal and spatial dimensions. The framework integrates clonal evolution dynamics, preexisting castration‑tolerant progenitors, fibroblast‑dominated barriers and metabolic crosstalk that collectively enforce immune evasion. Key therapeutic vulnerabilities, including YAP1‑TGF‑β1 axis disruption, PKMYT1 inhibition, metabolic targeting and biomarker‑guided patient stratification, are critically evaluated within this ecological context. Ultimately, the present review aimed to establish spatiotemporal co‑evolution as a unifying framework that transforms mCRPC from a uniformly fatal disease into a chronically manageable condition through precisely timed, spatially informed and mechanistically rational interventions.","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/PMC13614617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038524","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}

引用次数: 0

[Expression of Concern] Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1. [表达担忧]雷帕霉素诱导的miR - 30a下调通过靶向Beclin1抑制VSMCs衰老。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-11 DOI: 10.3892/ijmm.2026.5981

Pan Tan, Haiqin Wang, Junkun Zhan, Xinyu Ma, Xingjun Cui, Yanjiao Wang, Yi Wang, Jiayu Zhong, Youshuo Liu

{"title":"[Expression of Concern] Rapamycin‑induced miR‑30a downregulation inhibits senescence of VSMCs by targeting Beclin1.","authors":"Pan Tan, Haiqin Wang, Junkun Zhan, Xinyu Ma, Xingjun Cui, Yanjiao Wang, Yi Wang, Jiayu Zhong, Youshuo Liu","doi":"10.3892/ijmm.2026.5981","DOIUrl":"10.3892/ijmm.2026.5981","url":null,"abstract":"Following the publication of the above paper, it was drawn to the Editor's attention by an interested reader that a pair of unsuitable antibodies may have been used as a part of the western blot analysis shown in Fig. 1E on p. 1314. First, the antibody with the catalogue number ab51243 (purchased from Abcam), is not specific for p16‑INK4a (the senescence‑associated protein studied in this paper), but a totally different protein with a similar name, p16‑ARC. A concern was also raised regarding the anti‑β‑galactosidase antibody (cat. no. ab9361; Abcam) that was employed, which is specific for the bacterial protein and is only distantly related to human β‑galactosidase according to its sequence (neither is this antibody the closest homologue to bacterial β‑galactosidase in the human proteome). The authors have been contacted by the Editorial Office to offer an explanation for the selection of these apparently unsuitable antibodies for the western blot analysis, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of a potential problem surrounding the design of these experiments in this study, we are issuing an Expression of Concern to notify readers of this issue while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 43: 1311‑1320, 2019; DOI: 10.3892/ijmm.2019.4074].","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/PMC13592806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148944635","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}

引用次数: 0

Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review). 中暑中的铁下垂：机制和治疗观点（综述）。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-11 DOI: 10.3892/ijmm.2026.5984

Hongguang Gao, Yang Chen, Tianshan Zhang, Yujun Shi, Rong Yao

引用次数: 0

Research progress on BTG2 in non‑tumor diseases (Review). BTG2在非肿瘤疾病中的研究进展（综述）

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-08-28 DOI: 10.3892/ijmm.2026.5970

Shuling Li, Xiaomei Liu, Zheng Zhang, Ling Yang, Yuxuan Li, Qiongdan Hu

{"title":"Research progress on BTG2 in non‑tumor diseases (Review).","authors":"Shuling Li, Xiaomei Liu, Zheng Zhang, Ling Yang, Yuxuan Li, Qiongdan Hu","doi":"10.3892/ijmm.2026.5970","DOIUrl":"10.3892/ijmm.2026.5970","url":null,"abstract":"The B‑cell translocation gene 2 (BTG2), originally identified as a tumor suppressor, has been extensively studied in oncology research. However, its multifaceted functions in non‑tumor diseases are still being recognized but not entirely understood. This review systematically synthesizes advances in the pivotal, context‑dependent roles of BTG2 in non‑tumor pathologies, including fibrotic, neurological, cardiovascular, inflammatory, metabolic and other systemic diseases. BTG2 is not merely a binary regulator but a context‑sensitive molecular hub. Specific disease microenvironments, cell types and pathological stages contribute to its biological impact, whether protective or pathogenic. For instance, BTG2 promotes protective microglial activation in Alzheimer's disease while exacerbating neuronal death in acute spinal cord injury. Mechanistically, BTG2 influences cell fate decisions involving apoptosis, senescence, inflammation and metabolism by integrating signals from various pathways at the intersection of major regulatory networks, such as the neuro‑immune‑epigenetic axis and the metabolic‑epigenetic‑fibrosis network. It has emerged as a promising dual‑purpose biomarker for disease diagnosis and prognosis, as well as a potential therapeutic target, owing to its dose‑sensitive expression and regulatory position. However, because of its functional duality, therapeutic targeting necessitates precise, context‑specific strategies. This review offers a novel, integrative perspective on BTG2 in non‑tumor biology, underscoring its implication as a key regulatory node with extensive translational potential.","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/PMC13553039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840089","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}

引用次数: 0

Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review). 自噬通过调节代谢重塑和PANoptosis来决定免疫细胞的命运。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/ijmm.2026.5978

Yanan Guo, Xinyue Zhou, Yixiao Tian, Dan Chen, Xiaofeng Xie, Bin Zhou, Yingxia Tian, Yaqing Zhang

{"title":"Autophagy determines the fate of immune cells by regulating metabolic remodeling and PANoptosis (Review).","authors":"Yanan Guo, Xinyue Zhou, Yixiao Tian, Dan Chen, Xiaofeng Xie, Bin Zhou, Yingxia Tian, Yaqing Zhang","doi":"10.3892/ijmm.2026.5978","DOIUrl":"10.3892/ijmm.2026.5978","url":null,"abstract":"Autophagy, as a core mechanism for maintaining cellular homeostasis, influences differentiation and functional activation of immune cells by regulating metabolic reprogramming. Crucially, autophagy serves as a molecular switch that precisely modulates differentiation and subsequent cell fate decisions. It achieves this by eliminating intracellular danger signals or key complexes, thereby determining whether immune cells undergo PANoptosis, an inflammatory death mode that integrates features of pyroptosis, apoptosis and necroptosis. The present review systematically discusses the regulatory role of autophagy in the developmental, differentiation and metabolic pathways of various immune cells. Furthermore, it elucidates the mechanistic details by which autophagy, and particularly mitophagy, dampens excessive PANoptosis activation through the elimination of danger signals (such as mitochondrial DNA and reactive oxygen species) or the degradation of PANoptosome components. Additionally, it clarifies the molecular mechanism by which autophagy dysregulation, induced by specific pathological conditions, leads to inflammatory responses and immunopathological damage. Overall, this review establishes the significance of the autophagy‑PANoptosis axis in the development and progression of autoimmune diseases and tumors, providing a solid theoretical foundation for the optimization and innovation of therapeutic strategies for these diseases.","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/PMC13557443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891193","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}

引用次数: 0

Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review). 代谢综合征的程序性细胞死亡：从分子机制到治疗策略（综述）

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/ijmm.2026.5977

Jialin Zhong, Maofu Zhang, Yafang Zheng, Cuicui Gong, Yasheng Deng, Lisha Sun, Dongqi Zhou, Qian Zhou, Qiu Chen

{"title":"Programmed cell death in metabolic syndrome: From molecular mechanisms to therapeutic strategies (Review).","authors":"Jialin Zhong, Maofu Zhang, Yafang Zheng, Cuicui Gong, Yasheng Deng, Lisha Sun, Dongqi Zhou, Qian Zhou, Qiu Chen","doi":"10.3892/ijmm.2026.5977","DOIUrl":"10.3892/ijmm.2026.5977","url":null,"abstract":"Metabolic syndrome (MetS) is a clinical syndrome primarily characterized by insulin resistance, integrating central obesity, hyperglycemia, hypertension and dyslipidemia. It is associated with increased risks of type 2 diabetes mellitus, non‑alcoholic fatty liver disease and atherosclerosis. Due to its high prevalence, complex pathogenesis and lack of effective treatments, MetS has become a notable global health issue. Current therapeutic approaches mainly emphasize weight reduction through caloric restriction and increased physical activity, or pharmacological interventions to improve lipid profiles, blood pressure and blood glucose; however, their efficacy remains suboptimal. Growing evidence indicates that programmed cell death (PCD), as a key driver of inflammation, serves a crucial role in the development and progression of MetS. The present review provides a comprehensive overview of recent advances in the understanding of how established and emerging forms of PCD contribute to MetS pathogenesis, including apoptosis, pyroptosis, autophagy, ferroptosis, necroptosis, PANoptosis and disulfidptosis. Particular emphasis is placed on their molecular mechanisms, tissue‑specific functions, regulatory crosstalk and therapeutic potential. Additionally, the present review discusses novel regulatory approaches and potential therapeutic strategies based on PCD network intervention, offering theoretical foundations and directions for developing innovative therapies to prevent and treat MetS and its complications.","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/PMC13557444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891489","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}

引用次数: 0

Salvianolic acid monomers against metastasis: Decoding the multilayered interception of EMT, angiogenesis and immune evasion (Review). 丹酚酸单体抗转移：解码EMT，血管生成和免疫逃避的多层拦截（综述）。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/ijmm.2026.5972

Shiting Jiang, Dan Liu, Tingting Wei, Qiwei Shi, Haowen Wang, Yidan Gao, Pingsu Mao, Wenli Yang

{"title":"Salvianolic acid monomers against metastasis: Decoding the multilayered interception of EMT, angiogenesis and immune evasion (Review).","authors":"Shiting Jiang, Dan Liu, Tingting Wei, Qiwei Shi, Haowen Wang, Yidan Gao, Pingsu Mao, Wenli Yang","doi":"10.3892/ijmm.2026.5972","DOIUrl":"10.3892/ijmm.2026.5972","url":null,"abstract":"Salvianolic acids (SAs), a water‑soluble active component extracted from the traditional Chinese herb Salvia miltiorrhiza, have attracted considerable attention as an anti‑tumor agent. Accumulating evidence demonstrates that SAs potently inhibit tumor‑cell migration, invasion and metastasis through multiple signaling pathways and molecular targets. First, SAs remodel the extracellular matrix and suppress matrix metalloproteinase activities, thereby attenuating the epithelial‑mesenchymal transition and the associated stem‑like properties of cancer cells. Second, SAs block tumor angiogenesis, depriving tumors of essential nutrients and routes for metastasis. Third, SAs reprogram the tumor microenvironment by modulating immune cells, enhancing immune cell infiltration and relieving immunosuppression, ultimately curbing tumor progression. Fourth, SAs target metastatic cellular plasticity and therapy resistance by disrupting cytoskeletal reorganization, impairing cell motility and reversing drug‑resistant phenotypes, thereby enhancing cancer treatment efficacy with reduced toxicity. At the molecular level, SAs suppress the PI3K/AKT, MAPK and TGF‑β1/Smad signaling cascades, thereby diminishing the invasive and migratory capacity of tumor cells. In this review, recent advances in understanding the anti‑metastatic effects and underlying mechanisms of SAs were systematically summarized, the challenges hindering their clinical translation were discussed and future directions that may facilitate their development as a promising anti‑metastatic therapeutic agent were outlined.","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/PMC13553040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891469","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}

引用次数: 0

[Expression of Concern] Ginsenoside Rg1 protects against H2O2‑induced neuronal damage due to inhibition of the NLRP1 inflammasome signalling pathway in hippocampal neurons in vitro. 【关注表达】人参皂苷Rg1通过抑制体外海马神经元NLRP1炎性体信号通路，保护H2O2诱导的神经元损伤。

IF 8.5 3区医学

International journal of molecular medicine Pub Date : 2026-11-01 Epub Date: 2026-09-18 DOI: 10.3892/ijmm.2026.5988

Tan-Zhen Xu, Xiao-Yan Shen, Ling-Ling Sun, Ya-Li Chen, Bi-Qiong Zhang, Da-Ke Huang, Wei-Zu Li

{"title":"[Expression of Concern] Ginsenoside Rg1 protects against H2O2‑induced neuronal damage due to inhibition of the NLRP1 inflammasome signalling pathway in hippocampal neurons in vitro.","authors":"Tan-Zhen Xu, Xiao-Yan Shen, Ling-Ling Sun, Ya-Li Chen, Bi-Qiong Zhang, Da-Ke Huang, Wei-Zu Li","doi":"10.3892/ijmm.2026.5988","DOIUrl":"10.3892/ijmm.2026.5988","url":null,"abstract":"Following the publication of the above paper, it was drawn to the Editor's attention by an interested reader that an unsuitable antibody may have been used as a part of the western blot analysis shown in Fig. 3A on p. 720. The anti‑β‑galactosidase antibody (cat. no. ab9361; Abcam) that was employed, which is specific for the E. coli β‑galactosidase encoded by the LacZ gene; is only distantly related to the human protein, and would not necessarily be expected to bind to it. The authors have been contacted by the Editorial Office to offer an explanation for the selection of this apparently unsuitable antibody for the western blot analysis, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of a potential problem surrounding the design of this experiment in this study, we are issuing an Expression of Concern to notify readers of this issue while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 43: 717‑726, 2019; DOI: 10.3892/ijmm.2018.4005].","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/PMC13600328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989958","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}

引用次数: 0