DJ-1 activates the AMPK/mTOR pathway by binding RACK1 to induce autophagy and protect the myocardium from ischemia/hypoxia injury.

Biochem Biophys Res Commun

Provincial Key Laboratory of Basic Pharmacology, Nanchang University, Nanchang, Jiangxi, 330006, PR China. Electronic address:

Published: December 2022


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Article Abstract

Myocardial Ischemic Injury is a serious threat to human health, and DJ-1 is involved in cardioprotection. The research intended to explore the effects and mechanism of DJ-1 to protect myocardium against ischemia injury. DJ-1 overexpression lentivirus vectors were transduced into the myocardium of SD rats and H9c2 cells, and an AMI model in vivo and a hypoxia model in vitro were established, respectively. Results showed that DJ-1 overexpression alleviated myocardial ischemia injury, as demonstrated by reduced the extent of myocardial infarction, improved cell survival, decreased LDH activity and CK-MB release. Furthermore, DJ-1 interacted with RACK1, activated AMPK/mTOR pathway, induced adaptive autophagy and protected the myocardium. However, RACK1 siRNA or compound C (an AMPK inhibitor) could weaken the above effect of DJ-1 on myocardium. In conclusion, DJ-1 could activate adaptive autophagy by the RACK1/AMPK/mTOR pathway and protect the myocardium against ischemia injury.

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http://dx.doi.org/10.1016/j.bbrc.2022.10.100DOI Listing

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