{"title":"肠道微生物衍生代谢物作为线粒体功能障碍驱动的肠道炎症性疾病的潜在治疗药物","authors":"Gayatri Reghu, Pardhipa Nandigam, Ashna Fathima, Trinath Jamma","doi":"10.1155/cmi/9644892","DOIUrl":null,"url":null,"abstract":"<p>Inflammatory bowel diseases are a group of chronic diseases with increasing global incidence and rising morbidity and mortality, contributing to a significant health burden. Mainstream treatments for IBD are focused on controlling inflammation and alleviating the symptoms, also aiming for intestinal barrier repair. Understanding the cellular and molecular mechanisms underlying intestinal inflammatory disorders is the key to developing more targeted therapies to treat IBD. The growth, differentiation, and proliferation of intestinal epithelial cells require energy. Since mitochondria provide the energy also required for intestinal epithelial cells to maintain homeostasis and barrier integrity, their dysfunction can lead to cell death and inflammation. While several studies have confirmed the link between gut microbial metabolites and mitochondrial function, conflicting results from studies in IBD models have presented challenges to a detailed understanding of this area. This review focuses on presenting data from existing literature and highlighting the therapeutic potential of gut microbiota–derived metabolites in restoring mitochondrial function, which may likely develop into therapeutic interventions in IBD.</p><p><b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT01473524, NCT03724175</p>","PeriodicalId":9844,"journal":{"name":"Cellular Microbiology","volume":"2025 1","pages":""},"PeriodicalIF":1.6000,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cmi/9644892","citationCount":"0","resultStr":"{\"title\":\"Gut Microbiota–Derived Metabolites as Potential Therapeutics in Mitochondrial Dysfunction-Driven Intestinal Inflammatory Diseases\",\"authors\":\"Gayatri Reghu, Pardhipa Nandigam, Ashna Fathima, Trinath Jamma\",\"doi\":\"10.1155/cmi/9644892\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Inflammatory bowel diseases are a group of chronic diseases with increasing global incidence and rising morbidity and mortality, contributing to a significant health burden. Mainstream treatments for IBD are focused on controlling inflammation and alleviating the symptoms, also aiming for intestinal barrier repair. Understanding the cellular and molecular mechanisms underlying intestinal inflammatory disorders is the key to developing more targeted therapies to treat IBD. The growth, differentiation, and proliferation of intestinal epithelial cells require energy. Since mitochondria provide the energy also required for intestinal epithelial cells to maintain homeostasis and barrier integrity, their dysfunction can lead to cell death and inflammation. While several studies have confirmed the link between gut microbial metabolites and mitochondrial function, conflicting results from studies in IBD models have presented challenges to a detailed understanding of this area. This review focuses on presenting data from existing literature and highlighting the therapeutic potential of gut microbiota–derived metabolites in restoring mitochondrial function, which may likely develop into therapeutic interventions in IBD.</p><p><b>Trial Registration:</b> ClinicalTrials.gov identifier: NCT01473524, NCT03724175</p>\",\"PeriodicalId\":9844,\"journal\":{\"name\":\"Cellular Microbiology\",\"volume\":\"2025 1\",\"pages\":\"\"},\"PeriodicalIF\":1.6000,\"publicationDate\":\"2025-08-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1155/cmi/9644892\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cellular Microbiology\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1155/cmi/9644892\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular Microbiology","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1155/cmi/9644892","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
Gut Microbiota–Derived Metabolites as Potential Therapeutics in Mitochondrial Dysfunction-Driven Intestinal Inflammatory Diseases
Inflammatory bowel diseases are a group of chronic diseases with increasing global incidence and rising morbidity and mortality, contributing to a significant health burden. Mainstream treatments for IBD are focused on controlling inflammation and alleviating the symptoms, also aiming for intestinal barrier repair. Understanding the cellular and molecular mechanisms underlying intestinal inflammatory disorders is the key to developing more targeted therapies to treat IBD. The growth, differentiation, and proliferation of intestinal epithelial cells require energy. Since mitochondria provide the energy also required for intestinal epithelial cells to maintain homeostasis and barrier integrity, their dysfunction can lead to cell death and inflammation. While several studies have confirmed the link between gut microbial metabolites and mitochondrial function, conflicting results from studies in IBD models have presented challenges to a detailed understanding of this area. This review focuses on presenting data from existing literature and highlighting the therapeutic potential of gut microbiota–derived metabolites in restoring mitochondrial function, which may likely develop into therapeutic interventions in IBD.
期刊介绍:
Cellular Microbiology aims to publish outstanding contributions to the understanding of interactions between microbes, prokaryotes and eukaryotes, and their host in the context of pathogenic or mutualistic relationships, including co-infections and microbiota. We welcome studies on single cells, animals and plants, and encourage the use of model hosts and organoid cultures. Submission on cell and molecular biological aspects of microbes, such as their intracellular organization or the establishment and maintenance of their architecture in relation to virulence and pathogenicity are also encouraged. Contributions must provide mechanistic insights supported by quantitative data obtained through imaging, cellular, biochemical, structural or genetic approaches.