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Recent work found that the active form of DJ-1 was induced in the ischemic heart as an endogenous mechanism to attenuate glycative stress\u2014the 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\u2013reperfusion (I\/R) injury. Initial studies found that DJ-1 localized to the mitochondria and increased its interaction with Complex I and Complex III 3\u00a0days after the onset of myocardial I\/R injury. Next, we investigated the role DJ-1 plays in modulating glycative stress in the mitochondria. Analysis revealed that compared to wild-type control mice, mitochondria from DJ-1 deficient (DJ-1 KO) hearts showed increased levels of glycative stress following I\/R. Additionally, Complex I and Complex III glycation were found to be at higher levels in DJ-1 KO hearts. This corresponded with reduced complex activities, as well as reduced mitochondrial oxygen consumption ant ATP synthesis in the presence of pyruvate and malate. To further determine if DJ-1 influenced the glycation of the complexes, an adenoviral approach was used to over-express the active form of DJ-1(AAV9-DJ1\u0394C). Under I\/R conditions, the glycation of Complex I and Complex III were attenuated in hearts treated with AAV9-DJ1\u0394C. This was accompanied by improvements in complex activities, oxygen consumption, and ATP production. Together, this data suggests that cardiac DJ-1 maintains Complex I and Complex III efficiency and mitochondrial function during the recovery from I\/R injury. In elucidating a specific mechanism for DJ-1\u2019s role in the post-ischemic heart, these data break new ground for potential therapeutic strategies using DJ-1 as a target.<\/jats:p>","DOI":"10.1038\/s41598-021-98722-1","type":"journal-article","created":{"date-parts":[[2021,9,30]],"date-time":"2021-09-30T10:30:41Z","timestamp":1632997841000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart"],"prefix":"10.1038","volume":"11","author":[{"given":"Yvanna","family":"Pantner","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rohini","family":"Polavarapu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lih-Shen","family":"Chin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lian","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuuki","family":"Shimizu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John W.","family":"Calvert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,9,30]]},"reference":[{"key":"98722_CR1","doi-asserted-by":"publisher","first-page":"e005375","DOI":"10.1161\/CIRCOUTCOMES.118.005375","volume":"12","author":"AN Nowbar","year":"2019","unstructured":"Nowbar, A. 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