ArticleScientific reports2021
DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Novel Allogeneic Mitochondria and Associated Organelle Complex Treatment Prevents Myocardial Ischemia-Reperfusion Injury Through Anti-Apoptotic Effects.JACC. Asia · 2026Article
- Article
- Effects of protein glycation and protective mechanisms against glycative stress.Current opinion in pharmacology · 2024Review
- Chronic circadian rhythm disorder induces heart failure with preserved ejection fraction-like phenotype through the Clock-sGC-cGMP-PKG1 signaling pathway.Scientific reports · 2024Article
- DJ-1 as a Novel Therapeutic Target for Mitigating Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2024Review
- Progressive Motor and Non-Motor Symptoms inInternational journal of molecular sciences · 2023Article
- Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice.Scientific reports · 2022Article
- Hydrogen Sulfide Attenuates Lymphedema Via the Induction of Lymphangiogenesis Through a PI3K/Akt-Dependent Mechanism.Journal of the American Heart Association · 2022Article
- Autophagy and Glycative Stress: A Bittersweet Relationship in Neurodegeneration.Frontiers in cell and developmental biology · 2021Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
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. 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-DJ1ΔC). Under I/R conditions, the glycation of Complex I and Complex III were attenuated in hearts treated with AAV9-DJ1ΔC. 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's role in the post-ischemic heart, these data break new ground for potential therapeutic strategies using DJ-1 as a target.
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