脂肪变性
平衡
粒体自噬
氧化应激
线粒体
脂肪肝
能量稳态
线粒体生物发生
生物
内科学
内分泌学
细胞生物学
脂肪性肝炎
医学
自噬
生物化学
细胞凋亡
疾病
肥胖
作者
Yufeng Li,Zhifu Xie,Qian Song,Jing-Ya Li
标识
DOI:10.1038/s41401-022-00864-z
摘要
Mitochondrial biology and behavior are central to the physiology of liver. Multiple mitochondrial quality control mechanisms remodel mitochondrial homeostasis under physiological and pathological conditions. Mitochondrial dysfunction and damage induced by overnutrition lead to oxidative stress, inflammation, liver cell death, and collagen production, which advance hepatic steatosis to nonalcoholic steatohepatitis (NASH). Accumulating evidence suggests that specific interventions that target mitochondrial homeostasis, including energy metabolism, antioxidant effects, and mitochondrial quality control, have emerged as promising strategies for NASH treatment. However, clinical translation of these findings is challenging due to the complex and unclear mechanisms of mitochondrial homeostasis in the pathophysiology of NASH.
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