Acute exercise-induced mitochondrial stress triggers an inflammatory response in the myocardium via nlrp3 inflammasome activation with mitophagy

Haiying Li, Weiguo Miao, Jingfen Ma, Zhen Xv, Hai Bo, Jianyu Li, Yong Zhang, Li Li Ji

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

Increasing evidence has indicated that acute strenuous exercise can induce a range of adverse reactions including oxidative stress and tissue inflammation. However, little is currently known regarding the mechanisms that underlie the regulation of the inflammatory response in the myocardium during acute heavy exercise. This study evaluated the mitochondrial function, NLRP3 inflammasome activation, and mitochondrial autophagy-related proteins to investigate the regulation and mechanism of mitochondrial stress regarding the inflammatory response of the rat myocardium during acute heavy exercise. The results indicated that the mitochondrial function of the myocardium was adaptively regulated to meet the challenge of stress during acute exercise. The exercise-induced mitochondrial stress also enhanced ROS generation and triggered an inflammatory reaction via the NLRP3 inflammasome activation. Moreover, the mitochondrial autophagy-related proteins including Beclin1, LC3, and Bnip3 were all significantly upregulated during acute exercise, which suggests that mitophagy was stimulated in response to the oxidative stress and inflammatory response in the myocardium. Taken together, our data suggest that, during acute exercise, mitochondrial stress triggers the rat myocardial inflammatory response via NLRP3 inflammasome activation and activates mitophagy to minimize myocardial injury.

Original languageEnglish (US)
Article number1987149
JournalOxidative medicine and cellular longevity
Volume2016
DOIs
StatePublished - 2016

Bibliographical note

Publisher Copyright:
© 2016 Haiying Li et al.

Fingerprint

Dive into the research topics of 'Acute exercise-induced mitochondrial stress triggers an inflammatory response in the myocardium via nlrp3 inflammasome activation with mitophagy'. Together they form a unique fingerprint.

Cite this