ArticleJournal of the American Heart Association2020
Role of DJ-1 in Modulating Glycative Stress in Heart Failure.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021Guideline
- O-GlcNAcylation as a Metabolic Integrator in Cardiovascular Physiology and Disease.International journal of molecular sciences · 2026Review
- Adipose-derived regenerative cell therapy mitigates sepsis-induced cardiomyopathy through the induction of cardiac reparative lymphangiogenesis.Stem cell research & therapy · 2026Article
- Protein deglycase DJ-1 deficiency aggravates acute viral myocarditis by promoting apoptosis via reducing Dusp1 expression.Cell death & disease · 2025Article
- Sarcoplasmic reticulum-mitochondria microdomains: hugging and kissing in the heart.American journal of physiology. Cell physiology · 2025Review
- 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
- Cardiac Lymphatic Insufficiency Leads to Diastolic Dysfunction Via Myocardial Morphologic Change.JACC. Basic to translational science · 2023Article
- Metabolite signaling in the heart.Nature cardiovascular research · 2023Review
- Parkinson's disease and cardiovascular involvement: Edifying insights (Review).Biomedical reports · 2023Review
- Persulfidation of DJ-1: Mechanism and Consequences.Biomolecules · 2022Article
- DJ-1 interacts with the ectopic ATP-synthase in endothelial cells during acute ischemia and reperfusion.Scientific reports · 2022Article
- PARK7/DJ-1 as a Therapeutic Target in Gut-Brain Axis Diseases.International journal of molecular sciences · 2022Review
- Excess heme upregulates heme oxygenase 1 and promotes cardiac ferroptosis in mice with sickle cell disease.Blood · 2022Article
- DJ-1 administration exerts cardioprotection in a mouse model of acute myocardial infarction.Frontiers in pharmacology · 2022Article
- Glyoxylase-1 combats dicarbonyl stress and right ventricular dysfunction in rodent pulmonary arterial hypertension.Frontiers in cardiovascular medicine · 2022Article
- With No Lysine Kinase 1 Promotes Metabolic Derangements and RV Dysfunction in Pulmonary Arterial Hypertension.JACC. Basic to translational science · 2021Article
- DJ-1 attenuates the glycation of mitochondrial complex I and complex III in the post-ischemic heart.Scientific reports · 2021Article
- Cytoprotective Mechanisms of DJ-1: Implications in Cardiac Pathophysiology.Molecules (Basel, Switzerland) · 2021Review
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Background DJ-1 is a ubiquitously expressed protein typically associated with the development of early onset Parkinson disease. Recent data suggest that it also plays a role in the cellular response to stress. Here, we sought to determine the role DJ-1 plays in the development of heart failure. Methods and Results Initial studies found that DJ-1 deficient mice (DJ-1 knockout; male; 8-10 weeks of age) exhibited more severe left ventricular cavity dilatation, cardiac dysfunction, hypertrophy, and fibrosis in the setting of ischemia-reperfusion-induced heart failure when compared with wild-type littermates. In contrast, the overexpression of the active form of DJ-1 using a viral vector approach resulted in significant improvements in the severity of heart failure when compared with mice treated with a control virus. Subsequent studies aimed at evaluating the underlying protective mechanisms found that cardiac DJ-1 reduces the accumulation of advanced glycation end products and activation of the receptor for advanced glycation end products-thus, reducing glycative stress. Conclusions These results indicate that DJ-1 is an endogenous cytoprotective protein that protects against the development of ischemia-reperfusion-induced heart failure by reducing glycative stress. Our findings also demonstrate the feasibility of using a gene therapy approach to deliver the active form of DJ-1 to the heart as a therapeutic strategy to protect against the consequences of ischemic injury, which is a major cause of death in western populations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.