粒体自噬
线粒体
线粒体DNA
线粒体生物发生
线粒体融合
线粒体呼吸链
医学
线粒体ROS
DNAJA3公司
粒线体疾病
细胞生物学
TFAM公司
线粒体分裂
生物信息学
生物
自噬
氧化应激
内分泌学
细胞凋亡
遗传学
基因
作者
Shikun Yang,Yachun Han,Jun Liu,Panai Song,Xiaoxuan Xu,Li Zhao,Chun Hu,Li Xiao,Fuyou Liu,Hao Zhang,Lin Sun
标识
DOI:10.2174/0929867324666170509121003
摘要
BACKGROUND: Diabetic nephropathy (DN) is an important diabetic microvascular complication, and it is becoming the leading cause of end-stage renal disease worldwide. Unfortunately, there are no effective therapies to treat established DN. Therefore, new therapeutic targets are urgently required. Accumulating studies indicate that mitochondrial dysfunction is central to the pathogenesis of DN, and therapies targeted mitochondria might effectively delay the progression of DN. METHOD: A structured search of previously research literature about mitochondrial structure and function, mitochondrial DNA, mitochondrial biogenesis, mitochondrial dynamics change, mitophagy, mitochondrial ROS, mitochondrial apoptosis and therapies targeted mitochondria has been performed in several databases. RESULT: 176 papers were included in this review, the results from these papers indicated that mitochondrial dysfunction is a pivotal issue for the development of DN, such as elevated oxidative stress induced by disorders of the mitochondrial respiratory chain complex and mitochondrial dynamic disorders, mutation of mitochondrial DNA, mitochondrial abnormal biogenesis, mitochondrial excessive fission, mitochondrial ROS overproduction. In addition, several therapeutic agents targeting the mitochondria (e.g mitochondrial ROS modulators, mitochondrial fragmentation inhibitors and mitochondrial biogenesis activators) have shown perfect therapeutic effect and security for DN. CONCLUSION: The finding of this review has further confirmed the vital role of mitochondrial dysfunction in the progression of DN, management strategies for recovering the normal mitochondrial function will offer potential novel therapeutic targets for DN.
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