Overcoming mitochondrial dysfunction in neurodegenerative diseases
Jo?o Pessoa
Ana I.Duarte
CNC–Center for Neuroscience and Cell Biology,CIBB–Center for Innovative Biomedicine and Biotechnology,University of Coimbra,Coimbra,Portugal
摘要：Due to their intense electrical activity, neurons have high energy demands. This requirement makes them particularly sensitive to mitochondrial dysfunction. Like all eukaryotic cells, neurons have intrinsic mechanisms to mitigate the impact of mitochondrial dysfunction and its consequent production of toxic substances. Among such (neuro)protective mechanisms, mitochondrial autophagy (mitophagy) is responsible for the removal of dysfunctional mitochondria. Pathological inhibition of mitophagy, together with insufficient mitochondrial activity, results in a shortage of adenosine triphosphate (ATP) and the accumulation of reactive oxygen species (ROS) (Simmons et al., 2020). These alterations may trigger extensive apoptotic neuronal death (Figure 1A) which, together with the post-mitotic nature of neurons, impedes the replacement of the apoptotic cells.
机标关键词：neuroddegenerativediseasesdysfunctionmitochondrialovercoming
论文发表日期：2023-07-28
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：3( 1486-1488 )