S100A9 as a Key Myocardial Injury Factor Interacting with ATP5 Exacerbates Mitochondrial Dysfunction and Oxidative Stress in Sepsis-Induced Cardiomyopathy.
Hui PeiJie QuJianming ChenGuangju ZhaoZhong-Qiu LuPublished in: Journal of inflammation research (2024)
The interaction of S100A9 with ATP5 exacerbates myocardial damage in sepsis by inducing mitochondrial dysfunction and oxidative stress.