肠道菌群
疾病
线粒体
生物
机制(生物学)
分子医学
肾
生物信息学
微生物学
医学
免疫学
病理
细胞凋亡
细胞生物学
内分泌学
生物化学
哲学
认识论
细胞周期
作者
Leilei Ma,Li Zhang,Jing Li,Xiaotian Zhang,Yiran Xie,Xiaochen Li,Bo Yang,Hongtao Yang
标识
DOI:10.1186/s10020-023-00745-z
摘要
Abstract Diabetic kidney disease (DKD), has become the main cause of end-stage renal disease (ESRD) worldwide. Lately, it has been shown that the onset and advancement of DKD are linked to imbalances of gut microbiota and the abnormal generation of microbial metabolites. Similarly, a body of recent evidence revealed that biological alterations of mitochondria ranging from mitochondrial dysfunction and morphology can also exert significant effects on the occurrence of DKD. Based on the prevailing theory of endosymbiosis, it is believed that human mitochondria originated from microorganisms and share comparable biological characteristics with the microbiota found in the gut. Recent research has shown a strong correlation between the gut microbiome and mitochondrial function in the occurrence and development of metabolic disorders. The gut microbiome’s metabolites may play a vital role in this communication. However, the relationship between the gut microbiome and mitochondrial function in the development of DKD is not yet fully understood, and the role of microbial metabolites is still unclear. Recent studies are highlighted in this review to examine the possible mechanism of the gut microbiota-microbial metabolites-mitochondrial axis in the progression of DKD and the new therapeutic approaches for preventing or reducing DKD based on this biological axis in the future.
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