串扰
自噬
败血症
急性肾损伤
线粒体
病态的
细胞凋亡
病理生理学
生物
碎片(计算)
细胞生物学
医学
免疫学
内科学
生物化学
内分泌学
物理
光学
生态学
作者
Zhixiong Wu,Wei Liu,Liang Tang,Qiong Yuan,Yaling Li,Hongyu Hu,Xin Luo,Fan Ouyang
摘要
Abstract Independent risk factors for sepsis‐associated acute kidney injury (S‐AKI) patients include elevated lactate levels, but the specific mechanism remains unclear. Recently, An et al. discovered that excessive acetylation and inactivation of PDHA1 lead to overproduction of lactate, resulting in mitochondrial fragmentation, ATP depletion, excessive mtROS production, and mitochondrial apoptosis, thereby exacerbating AKI in sepsis. Therefore, understanding the pathophysiological processes of mitochondrial function and lactate generation in SAKI is essential and can aid in the development of novel therapeutic strategies. This review elucidates the pathological mechanisms of mitochondrial autophagy and dynamics in AKI. We also discuss the sources of lactate in SAKI and some consequences of lactonization, which may provide new strategies for improving renal injury and delaying the progression of these diseases.
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