This work examines the pathogenesis of angiotensin II (Ang-II)-induced muscle wasting. The authors show that Ang II increases NLRP3 inflammasome activation and mitochondrial reactive oxygen species generation. Additionally, PPAR-γ agonist can protect against Ang II-induced muscle wasting by preventing mitochondrial dysfunction (MtD), oxidative stress, and NLRP3 inflammasome activation. Targeting the PPAR-γ/MtD/NLRP3 inflammasome axis may therefore provide a therapeutic approach for muscle wasting.
- Yuqing Liu
- Xiao Bi
- Wei Ding
