粒体自噬
帕金
品脱1
自噬
线粒体
PTEN公司
发病机制
细胞生物学
机制(生物学)
信号转导
生物
医学
神经科学
PI3K/AKT/mTOR通路
免疫学
疾病
帕金森病
遗传学
内科学
细胞凋亡
哲学
认识论
作者
Xiao Yang,Weinan Pan,Gaolian Xu,Linxi Chen
标识
DOI:10.1016/j.cca.2019.11.008
摘要
Mitophagy is an autophagic process through which damaged or dysfunctional mitochondria are specifically degraded to maintain cellular homeostasis. It is highly regulated by various signaling pathways such as the PTEN-induced putative kinase 1 (PINK1)/Parkin and NIP3-like protein X (NIX)/BNIP3 pathways. Additionally, it plays a crucial role in inducing some pathological processes. Notably, some evidence suggesting the association of mitophagy with the occurrence of chronic diseases such as Parkinson's disease (PD), cancer, diabetes, atherosclerosis (AS), and myocardial ischemia reperfusion (MIR) injury is available. Particularly, it has been reported that mitophagy could hinder the development of PD by activating the PINK1/Parkin pathway and acting as a defense mechanism against the induction of diabetes. Conversely, the induction of mitophagy plays dual roles in driving the process of cancer, AS, and MIR injury. In this review, we have explained the role and regulatory mechanisms through which mitophagy plays a role in these chronic pathologies. Importantly, the pharmacological targeting of mitophagy might prove to be a potential alternative for the treatment of these chronic diseases.
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