DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart.

ABSTRACT: DJ-1 is a ubiquitously expressed protein that protects cells from stress through its conversion into an active protease. Recent work found that the active form of DJ-1 was induced in the ischemic heart as an endogenous mechanism to attenuate glycative stress-the non-enzymatic glycosylation of proteins. However, specific proteins protected from glycative stress by DJ-1 are not known. Given that mitochondrial electron transport proteins have a propensity for being targets of glycative stress, we investigated if DJ-1 regulates the glycation of Complex I and Complex III after myocardial ischemia-reperfusion (I/R) injury. Initial studies found that DJ-1 localized to the mitochondria and increased its interaction with Complex I and Complex III 3 days after the onset of myocardial I/R injury. Nex

SUBMITTER: Pantner Y 

PROVIDER: S-EPMC8484662 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature