粒体自噬
线粒体
脂肪生成
非酒精性脂肪肝
细胞生物学
氧化应激
自噬
生物
肝细胞
脂肪变性
平衡
脂质代谢
脂肪肝
化学
生物化学
内科学
内分泌学
医学
疾病
细胞凋亡
体外
作者
Nicolás Salva-Pastor,Mayra Domínguez‐Pérez,Norberto C. Chávez-Tapia,Natalia Nuño‐Lámbarri
出处
期刊:Elsevier eBooks
[Elsevier BV]
日期:2021-01-01
标识
DOI:10.1016/b978-0-12-819621-2.00006-1
摘要
Abstract Under normal conditions, the liver performs a balance between lipogenesis and lipid degradation; however, lipid homeostasis is altered in hepatic steatosis, with fatty acids and triglycerides excess, which are stored inside the hepatocyte in the form of lipid vesicles. Mitochondria play an essential role in the oxidative metabolism of biomolecules and the maintenance of liver function; therefore, alterations in their function and structure generate oxidative stress that leads to different signaling pathways dysfunction, which contributes to nonalcoholic fatty liver disease development. Mitochondrial dynamics is responsible for regulating the proper functioning of mitochondria, both in physiological processes and in pathological conditions; it includes processes such as fusion, fission, biogenesis, mitophagy, and motility throughout the cell. On the other hand, autophagy is a cellular degradation pathway that maintains cell homeostasis and provides substrates for energy generation. Consequently, it is suggested that mitochondria may be the origin of injury fate.
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