The role of microbiota-mitochondria crosstalk in pathogenesis and therapy of intestinal diseases.
The role of microbiota-mitochondria crosstalk in pathogenesis and therapy of intestinal diseases.
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DOI：
10.1016/j.phrs.2022.106530
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发表时间：
2022-10
影响因子：
9.3
通讯作者：
Yiming Zhang;Jindong Zhang;L. Duan
中科院分区：
文献类型：
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作者：
Yiming Zhang;Jindong Zhang;L. Duan
线粒体和肠道微生物区系之间的相互作用在肠道生理动态平衡中起着关键作用。在这种动态平衡中，肠道上皮低氧有助于微生物区系由专性厌氧菌主导，这些厌氧菌为宿主提供有益的代谢物，如短链脂肪酸(SCFA)。此外，新出现的研究表明，微生物对肠上皮细胞线粒体的信号可以改变线粒体的超微结构及其代谢功能，诱导炎性小体激活，并破坏上皮细胞的缺氧。改变线粒体的条件可能会导致肠道上皮炎症和氧合，这两者都会导致兼性厌氧菌的扩张，并加剧线粒体-微生物区系的失衡。这一现象已被证明与胃肠道(GI)疾病的发病机制有关，包括炎症性肠病(IBD)和结直肠癌(CRC)。因此，本文综述了近年来在胃肠道生理动态平衡和疾病的情况下，肠内皮细胞线粒体与肠道微生物区系相互作用的研究进展，以及针对线粒体-微生物区系串扰在胃肠道疾病中的潜在治疗干预。
The interaction between mitochondria and gut microbiota plays a critical role in intestinal physiological homeostasis. In this kind of homeostasis, intestinal epithelial hypoxia helps microbiota to be dominated by obligate anaerobes, who provide their benefit metabolites for the host, such as short chain fatty acids (SCFAs). In addition, emerging studies suggest that microbial signals to the mitochondria of intestinal epithelial cells (IECs) could alter mitochondrial ultrastructure and its metabolic function, induce inflammasome activation and disrupt epithelial hypoxia. Conditions that alter the mitochondria could lead to intestinal epithelium inflammation and oxygenation, both of which would drive an expansion of facultative anaerobes and exacerbate the imbalance of mitochondria-microbiota crosstalk. This phenomenon has proved to be associated with the pathogenesis of gastrointestinal (GI) diseases, including inflammatory bowel disease (IBD) and colorectal cancer (CRC). Therefore, in this review, we summarized the recent process on the interaction between mitochondria of IECs and gut microbiota in the case of both GI physiological homeostasis and diseases, and potential therapeutic interventions targeting mitochondria-microbiota crosstalk in GI diseases.