ArticleFrontiers in cardiovascular medicine2022
MG53 Inhibits Necroptosis Through Ubiquitination-Dependent RIPK1 Degradation for Cardiac Protection Following Ischemia/Reperfusion Injury.
Article in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 22 citations in OpenAlex.
- MG53 Coordinates Macrophage Polarization and Neuroimmune Coupling to Promote Corneal Nerve Regeneration via the MPEG1-MVP-STAT6 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- OGT-mediated O-GlcNAcylation Protects Against Myocardial Ischemia-Reperfusion Injury via Targeting MG53.Applied biochemistry and biotechnology · 2026Article
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- MG53 in Early Skeletal Muscle Stem Cell Activation: Implications for Aged Muscle Regeneration.Cells · 2026Review
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- Necroptosis in myocardial ischaemia-reperfusion injury: current update on mechanisms, therapeutic targets, and translational potential.Apoptosis : an international journal on programmed cell death · 2025Review
- The Role of Post-Translational Modifications in Necroptosis.Biomolecules · 2025Review
- YTHDF2 mediates the protective effects of MG53 on myocardial infarction injury via recognizing the m6A modification of MG53.Journal of cardiothoracic surgery · 2025Article
- USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377.Research (Washington, D.C.) · 2025Article
- Mitsugumin 53 mitigation of ischemia-reperfusion injury in a mouse model.The Journal of thoracic and cardiovascular surgery · 2024Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- The Next Frontier in Lung Transplantation: Protecting the Endothelium and Repairing Organs for Transplant Utilizing MG53.Clinical and translational discovery · 2023Article
- Activation of MG53 Enhances Cell Survival and Engraftment of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes in Injured Hearts.Stem cell reviews and reports · 2023Article
- Review
- Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Review
- Advances in the Study of MG53 in Cardiovascular Disease.International journal of general medicine · 2023Review
- Protective role of MG53 against ischemia/reperfusion injury on multiple organs: A narrative review.Frontiers in physiology · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Rationale: While reactive oxygen species (ROS) has been recognized as one of the main causes of cardiac injury following myocardial infarction, the clinical application of antioxidants has shown limited effects on protecting hearts against ischemia-reperfusion (I/R) injury. Thus, the precise role of ROS following cardiac injury remains to be fully elucidated. Objective: We investigated the role of mitsugumin 53 (MG53) in regulating necroptosis following I/R injury to the hearts and the involvement of ROS in MG53-mediated cardioprotection. Methods and Results: Antioxidants were used to test the role of ROS in MG53-mediated cardioprotection in the mouse model of I/R injury and induced human pluripotent stem cells (hiPSCs)-derived cardiomyocytes subjected to hypoxia or re-oxygenation (H/R) injury. Western blotting and co-immunoprecipitation were used to identify potential cell death pathways that MG53 was involved in. CRISPR/Cas 9-mediated genome editing and mutagenesis assays were performed to further identify specific interaction amino acids between MG53 and its ubiquitin E3 ligase substrate. We found that MG53 could protect myocardial injury Conclusions: Taken together, this study provided a molecular mechanism of a potential beneficial role of ROS following acute myocardial infarction. Thus, fine-tuning ROS levels might be critical for cardioprotection.
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Registered trials
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