Oxidative-Damaged Mitochondria Activate GABARAPL1-Induced NLRP3 Inflammasomes in an Autophagic-Exosome Manner after Acute Myocardial Ischemia.

Tiechun ZhangDongyao HouJianrong HeXue ZengRuixue LiuLiangming LiuTao LiYingbin XiaoRuiyan Ma He Huang Chen-Yang Duan

Published in: Oxidative medicine and cellular longevity (2022)

Oxidative-damaged mitochondria in cardiac CMECs activate GEC1-mediated autophagosomes but block autophagy flux after AMI. The exfoliated cardiac CMECs evolve into abnormal blood CECs, and the undegraded GEC1 autophagosomes produce a large number of NLRP3 inflammasomes by exosome burst, stimulating the increase in monocytes and neutrophils and ultimately triggering vascular inflammation after AMI. Therefore, GEC1 in blood CECs is a highly specific diagnostic mitochondrial biomarker for AMI.

Keyphrases

cell death
acute myocardial infarction
left ventricular
oxidative stress
diabetic rats
reactive oxygen species
percutaneous coronary intervention
endoplasmic reticulum
heart failure
nlrp inflammasome
signaling pathway
high frequency
dendritic cells
peripheral blood
acute coronary syndrome