A partial Drp1 knockout improves autophagy flux independent of mitochondrial function.

Rebecca Z FanCarolina SportelliYanhao LaiSaid S SaleheJennifer R PinnellHarry J BrownJason R RichardsonShouqing LuoKim Tieu

Published in: Molecular neurodegeneration (2024)

This study demonstrates that improved autophagy flux is a separate mechanism conferred by Drp1 inhibition independent of its role in mitochondrial fission. Given that impaired autophagy and mitochondrial dysfunction are two prominent features of neurodegenerative diseases, the combined protective mechanisms targeting these two pathways conferred by Drp1 inhibition make this protein an attractive therapeutic target.

Keyphrases

cell death
oxidative stress
endoplasmic reticulum stress
signaling pathway
protein protein
small molecule
binding protein