Effects of mitophagy on cell death in Parkinson's disease model cells

PINK1/parkin介导的线粒体自噬通过每个基因表达的缺失和基因的致病性突变而减弱，并由PINK1在线粒体外膜上的积累触发。在PINK1-/-小鼠胚胎成纤维细胞中，线粒体功能不足，而活性氧的产生不变。咖啡因是一种众所周知的具有pd延迟作用的化学物质，通过增强自噬诱导细胞凋亡。唑尼沙胺通过抑制凋亡通路和诱导MnSOD表达来预防细胞死亡。

PINK1/parkin-mediated mitophagy is attenuated by loss of each gene expression and pathogenic mutations of the genes and is triggered by PINK1 accumulation on the mitochondrial outer membrane. In PINK1-/- mouse embryonic fibroblasts, mitochondrial function is insufficient, whilst production of the reactive oxygen species is unchanged.Caffeine, a well-known chemical with PD-onset retardation effects, induces apoptosis via enhancement of autophagy. Zonisamide prevents cell death via suppression of apoptotic pathway and induction of MnSOD expression.