Molecular medicine reports最新文献

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Multi‑omics approaches to decipher the molecular mechanisms of exercise‑mediated bone protection: From mechanistic insights to personalized exercise prescription (Review). 多组学方法解读运动介导的骨骼保护的分子机制:从机制见解到个性化运动处方(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/mmr.2026.14009
Bin Tian, Xuesong Chen, Xin Kang
{"title":"Multi‑omics approaches to decipher the molecular mechanisms of exercise‑mediated bone protection: From mechanistic insights to personalized exercise prescription (Review).","authors":"Bin Tian, Xuesong Chen, Xin Kang","doi":"10.3892/mmr.2026.14009","DOIUrl":"https://doi.org/10.3892/mmr.2026.14009","url":null,"abstract":"<p><p>The global burden of bone metabolic disorders necessitates a shift from generic exercise recommendations toward personalized prescription strategies. Exercise confers skeletal protection through mechanotransduction, yet the underlying molecular networks remain incompletely understood. Multi‑omics technologies, including transcriptomics, proteomics, metabolomics and single‑cell spatial approaches, have revolutionized the capacity to decode exercise‑mediated bone adaptation at the systems level. The present review synthesizes current single‑omics landscapes and integrative multi‑omics analyses that elucidate the core regulatory networks, mechanobiological coupling mechanisms and multiorgan crosstalk that are implicated in the bone response to mechanical loading. Translational applications across clinical scenarios such as osteoporosis, osteoarthritis and disuse bone loss are evaluated, and the technical, analytical and translational challenges limiting clinical implementation are addressed. Finally, the present review provides a framework for translating multi‑omics molecular signatures into personalized exercise prescriptions for optimized skeletal health.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Retracted] MicroRNA‑27a promotes tumorigenesis via targeting AKT in triple negative breast cancer. MicroRNA - 27a在三阴性乳腺癌中通过靶向AKT促进肿瘤发生
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-11-01 Epub Date: 2026-09-04 DOI: 10.3892/mmr.2026.14008
Jing Wu, Zhihui Sun, Huijie Sun, Yanhua Li
{"title":"[Retracted] MicroRNA‑27a promotes tumorigenesis via targeting AKT in triple negative breast cancer.","authors":"Jing Wu, Zhihui Sun, Huijie Sun, Yanhua Li","doi":"10.3892/mmr.2026.14008","DOIUrl":"https://doi.org/10.3892/mmr.2026.14008","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 certain of the cell migration and invasion data featured in Fig. 2C, G, H, K, L and O on p. 565‑6 were strikingly similar to data which appeared in a handful of other articles written by different authors at different research institutes, one of which had already been published in <i>Journal of Biological Research‑Thessaloniki</i> during the year before this paper was submitted to <i>Molecular Medicine Reports</i>. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 562‑570, 2018; DOI: 10.3892/mmr.2017.7886].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Mitochondrial quality control in acute liver injury and its therapeutic implications (Review). 急性肝损伤的线粒体质量控制及其治疗意义(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-07 DOI: 10.3892/mmr.2026.13984
Ziqiang Chen, Yunhe Wang, Yijing Li, Gang Cong, Yunhang Chu, Yunhui Bai, Yishuo Zhang, Liya Zhou
{"title":"Mitochondrial quality control in acute liver injury and its therapeutic implications (Review).","authors":"Ziqiang Chen, Yunhe Wang, Yijing Li, Gang Cong, Yunhang Chu, Yunhui Bai, Yishuo Zhang, Liya Zhou","doi":"10.3892/mmr.2026.13984","DOIUrl":"10.3892/mmr.2026.13984","url":null,"abstract":"<p><p>Acute liver injury (ALI) is a clinically important syndrome with limited mechanism‑based therapies. Notably, mitochondrial dysfunction is increasingly recognized as a central driver of hepatocellular damage and repair failure. The present narrative review aims to summarize the current evidence on mitochondrial quality control (MQC) in ALI, with an emphasis on mitophagy, mitochondrial biogenesis, mitochondrial dynamics, etiology‑specific regulation and therapeutic implications. For the present review, relevant experimental and translational studies addressing MQC‑related mechanisms and interventions in major forms of ALI, including drug‑induced liver injury, ischemia‑reperfusion injury and viral ALI, were reviewed and integrated. The findings indicated that MQC operates as an interconnected network rather than as isolated pathways. Mitophagy, mitochondrial dynamics and mitochondrial biogenesis are temporally coordinated to remove damaged mitochondria, remodel mitochondrial networks and restore bioenergetic capacity. However, MQC responses differ across ALI etiologies, and inappropriate or excessive activation may become maladaptive. In conclusion, understanding MQC as a dynamic and context‑dependent repair system may provide a conceptual basis for precision interventions in ALI. Future studies should clarify spatiotemporal MQC regulation, establish reliable biomarkers and validate MQC‑targeted therapies in clinically relevant settings.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13469799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685190","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
Gut microbiota‑immune crosstalk in recurrent pregnancy loss: Mechanisms and therapeutic perspectives (Review). 复发性妊娠丢失中的肠道微生物群-免疫串扰:机制和治疗观点(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-07 DOI: 10.3892/mmr.2026.13979
Nanjian Luo, Han Hu, Xiaoting Zeng, Yi Huan Zhang, Qi Deng, En Ni Tang, Yu Hu
{"title":"Gut microbiota‑immune crosstalk in recurrent pregnancy loss: Mechanisms and therapeutic perspectives (Review).","authors":"Nanjian Luo, Han Hu, Xiaoting Zeng, Yi Huan Zhang, Qi Deng, En Ni Tang, Yu Hu","doi":"10.3892/mmr.2026.13979","DOIUrl":"10.3892/mmr.2026.13979","url":null,"abstract":"<p><p>Recent studies have indicated the relationships between the human reproductive system, gut microbiota and immune crosstalk. These interactions can influence pregnancy outcomes, which occasionally result in adverse consequences for the mother and fetus. However, key questions remain unresolved, such as identifying the microbiota capable of modulating immune cells during pregnancy. The present review aimed to investigate the relationship between microbiota and T cell types and to clarify the mechanism through which these interactions occur. In pregnancy‑related disease models, it is still unclear whether T helper cell (Th17)/regulatory T cells (Treg cells) are generated <i>in situ</i> or migrate into inflamed tissues. The present review explored the association of gastrointestinal dysbiosis with the female reproductive system and the role of the maternal‑fetal interface. In particular, the effect of gut microbiota‑derived short‑chain fatty acids, bile acids, indoles and their derivatives on immune signaling networks is discussed. Furthermore, the effects of these networks on infectious, metabolic and female pregnancy periods are summarized. Finally, the translational potential of modulating gut microbiota through probiotics and dietary interventions to restore immune homeostasis and improve pregnancy outcomes in Recurrent pregnancy loss (RPL) is also evaluated. The present review aimed to assist patients in developing a more profound comprehension of the underlying causes of unexplained RPL and broaden the spectrum of potential therapeutic strategies for infertility.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13470128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685194","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
Interaction of circular RNAs with splicing factors in cervical cancer: Modulation, interplay and theranostics (Review). 环状rna与剪接因子在宫颈癌中的相互作用:调节、相互作用和治疗。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-09-04 DOI: 10.3892/mmr.2026.14006
Amahle Nyalambisa, Afra Basera, Ntombikayise Xelwa, Olalekan Fadebi, Zodwa Dlamini, Rahaba Marima
{"title":"Interaction of circular RNAs with splicing factors in cervical cancer: Modulation, interplay and theranostics (Review).","authors":"Amahle Nyalambisa, Afra Basera, Ntombikayise Xelwa, Olalekan Fadebi, Zodwa Dlamini, Rahaba Marima","doi":"10.3892/mmr.2026.14006","DOIUrl":"https://doi.org/10.3892/mmr.2026.14006","url":null,"abstract":"<p><p>Cervical cancer (CCa) is a worldwide health concern, particularly in low‑ and middle‑income countries. Human papillomavirus infection is a key risk factor in the development of CCa. Noncoding RNAs (ncRNAs), including microRNAs (miRNAs), circular RNAs (circRNAs) and long ncRNAs (lncRNAs), are important regulators of cancer progression, including CCa, offering potential therapeutic targets. Compared with lncRNAs and miRNAs, circRNAs are the least studied ncRNAs. circRNAs, distinguished by a closed‑loop structure and resistance to exonucleases, serve diverse roles in cancer, functioning as miRNA sponges and regulating gene expression. circRNAs are produced primarily by back‑splicing and comprise both intronic and exonic sequences. Notably, circRNAs are key regulators of alternative splicing, as they are able to enhance the expression of splicing factors (SFs) by sequestering miRNAs. Despite their importance, the interactions between circRNAs and SFs in CCa remain to be elucidated. The present review highlights the interplay between circRNAs and SFs in CCa pathogenesis; it describes the influence of SFs on circRNA production, the regulatory feedback between circRNAs and SFs, and the potential implications of this interaction in CCa diagnostics and therapeutics. To conduct the present review a targeted literature search was conducted across PubMed, Scopus and Google Scholar using defined search terms to identify peer‑reviewed studies published between 2006 and 2024. The findings were synthesized to explore the mechanistic insights and translational implications of circRNA‑SF interactions in CCa.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Advances in miR‑200c regulation of apoptosis, pyroptosis and autophagy in disease (Review). miR - 200c调控疾病中细胞凋亡、焦亡和自噬的研究进展(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-07-31 DOI: 10.3892/mmr.2026.13975
Xiaona Wang, Hua Du, Yingxu Shi
{"title":"Advances in miR‑200c regulation of apoptosis, pyroptosis and autophagy in disease (Review).","authors":"Xiaona Wang, Hua Du, Yingxu Shi","doi":"10.3892/mmr.2026.13975","DOIUrl":"10.3892/mmr.2026.13975","url":null,"abstract":"<p><p>MicroRNAs (miRNAs or miRs) represent conserved non‑coding RNAs responsible for the regulation of gene expression in a post‑transcriptional manner. The dysregulation of miRNAs often leads to disease development and progress. In particular, miR‑200c is one of the miR‑200 family members, which is found deregulated in various pathologies and involved in the process of cancer progression through its participation in different molecular signaling pathways. Initially, miR‑200c was regarded as an essential factor in metastases formation. Nevertheless, following the increase in knowledge about cell death signaling pathways, it became clear that miR‑200c participates in various types of cell death such as apoptosis, autophagy and pyroptosis. The present narrative review primarily discusses the molecular mechanisms through which miR‑200c regulates apoptosis, pyroptosis and autophagy and explores its potential therapeutic value.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13454991/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630869","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
Histone deacetylase 3‑mediated histone deacetylation combined with activating transcription factor 3 promotes renal fibrosis by inhibiting Klotho. 组蛋白去乙酰化酶3介导的组蛋白去乙酰化联合活化转录因子3通过抑制Klotho促进肾纤维化。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-07 DOI: 10.3892/mmr.2026.13985
Zhiying Yang, Xueling Wang, Wenhong Li, Hao Chen, Gang Liu
{"title":"Histone deacetylase 3‑mediated histone deacetylation combined with activating transcription factor 3 promotes renal fibrosis by inhibiting Klotho.","authors":"Zhiying Yang, Xueling Wang, Wenhong Li, Hao Chen, Gang Liu","doi":"10.3892/mmr.2026.13985","DOIUrl":"10.3892/mmr.2026.13985","url":null,"abstract":"<p><p>Renal fibrosis is a representative pathological trait of renal aging and chronic kidney disease. However, the regulatory mechanisms of histone deacetylation in renal fibrosis remain unclear. A mouse renal fibrosis model was constructed using the unilateral ureteric obstruction method, and HK2 cells treated with TGF‑β were used to create a renal fibrosis cell model. Low expression of Klotho in renal fibrosis is associated with histone deacetylase 3 (HDAC3)‑mediated histone deacetylation. After TGF‑β treatment, H3K9ac and Klotho binding was markedly decreased, while H3K9ac was enriched in the Klotho group after the addition of the HDAC3 inhibitor. Further experiments demonstrated that HDAC3 binding activates transcription factor 3, inhibits Klotho transcription and promotes cellular renal fibrosis. The absence of Klotho may activate the Wnt/β‑catenin and NF‑κB pathways to promote oxidative stress and inflammation, thereby exacerbating the fibrotic process. HDAC3 binds to ATF3 to transcriptionally repress Klotho, leading to activation of the Wnt/β‑catenin and NF‑κB pathways and exacerbation of renal fibrosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13488142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685214","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
Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review). 脑缺血再灌注损伤中线粒体功能障碍驱动的铁下垂:机制和治疗策略(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-21 DOI: 10.3892/mmr.2026.13997
Jianhui Li, Annan Liu, Wei Gao, Liping Xing, Peihan Duan, Honglin Li
{"title":"Mitochondrial dysfunction‑driven ferroptosis in cerebral ischemia‑reperfusion injury: Mechanisms and therapeutic strategies (Review).","authors":"Jianhui Li, Annan Liu, Wei Gao, Liping Xing, Peihan Duan, Honglin Li","doi":"10.3892/mmr.2026.13997","DOIUrl":"10.3892/mmr.2026.13997","url":null,"abstract":"<p><p>Ischemic stroke remains a leading cause of mortality and disability worldwide. Although vascular recanalization is essential for salvaging the ischemic penumbra, subsequent reperfusion may initiate a cascade of secondary brain injury, a pathological process referred to as cerebral ischemia‑reperfusion injury (CIRI). Ferroptosis, an iron‑dependent form of programmed cell death characterized by the excessive accumulation of lipid peroxides and membrane damage, has emerged as a critical driver of neuronal death in CIRI. Growing evidence supports mitochondrial dysfunction as not only a downstream outcome of bioenergetic failure, but also a central regulatory node within the ferroptotic cascade. The present review systematically summarizes how mitochondrial dysfunction increases neuronal susceptibility to ferroptosis across the pathophysiological progression of CIRI, with a particular focus on the underlying mechanisms. Specifically, a multidimensional pathological network composed of multiple mitochondrial abnormalities, including mitochondrial reactive oxygen species bursts, Ca2+ overload and disruption of the mitochondrial quality control system, encompassing mitochondrial biogenesis, mitochondrial dynamics and mitophagy, synergistically amplifies lipid peroxidation and drives neuronal ferroptosis. Finally, advances and future perspectives regarding mitochondria‑centered therapeutic strategies are highlighted, offering novel insights into the development of targeted neuroprotective interventions against CIRI‑induced ferroptosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795540","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
Unlocking the potential of microRNA as predictive biomarkers for efficacy and adverse events in immune checkpoint inhibitor therapy (Review). 解锁microRNA作为免疫检查点抑制剂治疗疗效和不良事件的预测性生物标志物的潜力(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-21 DOI: 10.3892/mmr.2026.13998
Xi Wang, Baojun Duan, Jun Bai, Huitong Liu
{"title":"Unlocking the potential of microRNA as predictive biomarkers for efficacy and adverse events in immune checkpoint inhibitor therapy (Review).","authors":"Xi Wang, Baojun Duan, Jun Bai, Huitong Liu","doi":"10.3892/mmr.2026.13998","DOIUrl":"10.3892/mmr.2026.13998","url":null,"abstract":"<p><p>Immune checkpoint inhibitors (ICIs) have shown promise in cancer therapy by enhancing antitumor immune responses, but patient responses are variable, with some experiencing limited efficacy and others suffering from severe immune‑related adverse events (irAEs). Identifying predictive biomarkers for ICI efficacy and toxicity is required for optimizing patient selection and treatment outcomes. MicroRNAs (miRNAs), small non‑coding RNA molecules that regulate gene expression, have emerged as potential biomarkers due to their role in immune regulation and tumor biology. Studies have shown that miRNA profiles in tumor tissues and blood can predict ICI responses. Specific miRNAs, such as miR‑155, miR‑21 and miR‑146a, are associated with enhanced antitumor responses, whereas others, such as miR‑34a and miR‑200c, are linked to resistance by modulating immune evasion. Additionally, altered miRNA expression reflects immune activation or dysregulation, playing a role in irAEs. The present review discussed the potential of miRNAs as predictive biomarkers for ICI therapy, their challenges in clinical integration and their promise for improving ICI treatment precision and safety, although further research is required for clinical application.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13504462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795554","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: Mechanisms and therapeutic perspectives in intestinal metaplasia (Review). 自噬:肠化生的机制和治疗前景(综述)。
IF 5 3区 医学
Molecular medicine reports Pub Date : 2026-10-01 Epub Date: 2026-08-21 DOI: 10.3892/mmr.2026.13999
Laifeng Wu, Lingchen Liao, Ziwei Xia, Qiao Zeng, An Huang, Zhiyong Cao
{"title":"Autophagy: Mechanisms and therapeutic perspectives in intestinal metaplasia (Review).","authors":"Laifeng Wu, Lingchen Liao, Ziwei Xia, Qiao Zeng, An Huang, Zhiyong Cao","doi":"10.3892/mmr.2026.13999","DOIUrl":"10.3892/mmr.2026.13999","url":null,"abstract":"<p><p>Intestinal metaplasia (IM) represents a key stage in the progression of gastric mucosal lesions to gastric cancer, marked by a complex molecular pathogenesis and a lack of effective interventional strategies. Autophagy, a key mechanism for maintaining cell homeostasis, is closely associated with the onset and progression of IM. The present review aimed to summarize the role of autophagy in IM by integrating its association with risk factors and pathogenic mechanisms. The present study evaluated the impact of autophagy on inflammation, immune responses and cellular fate determination during IM. The present study summarized potential autophagy‑mediated therapeutic agents for IM treatment and future research directions and existing limitations, aiming to provide novel insight for preventing and managing this premalignant condition.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13543149/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795575","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
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