ArticleRedox biology2022
MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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
46 citing papers in PubMed, 70 citations in OpenAlex.
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
- 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
- Metabolic Reprogramming-Driven Cardiovascular Immune Damage: From Glyco-Lipotoxicity and Epigenetic Memory to Multidimensional Cross-Organ Communication Networks.International journal of molecular sciences · 2026Review
- Cabozantinib activates TFEB-mediated autophagy to exert anti-tumor effects in hepatocellular carcinoma.In vitro cellular & developmental biology. Animal · 2026Article
- Decreased serum MG53 levels are associated with SHBG and androgen excess in women with polycystic ovary syndrome.Scientific reports · 2026Observational
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Baicalin Attenuates Oxidative Stress and Apoptosis in Myocardial Ischemia/reperfusion Injury via Suppression of STING/NLRP3 Pathway.Journal of cardiovascular translational research · 2026Article
- Exercise modulates redox homeostasis in cardiovascular and metabolic diseases: from bench to clinic.Cardiovascular diabetology · 2026Review
- Cytoskeletal remodeling promotes tunneling nanotube formation and drives cardiac resident cell mitochondrial transfer in sepsis.Science advances · 2026Article
- MG53 in Early Skeletal Muscle Stem Cell Activation: Implications for Aged Muscle Regeneration.Cells · 2026Review
- MG53 mediates skeletal muscle-liver cross-talk and enhances alcohol metabolism in alcoholic liver disease.Nature communications · 2026Article
- Dynamic microRNA Signatures as Biomarkers for Cardiac Ischemia and Remodeling.International journal of molecular sciences · 2026Article
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- TRIM52 Protects Against Doxorubicin-Induced Cardiac Inflammation, Oxidative Stress and Cardiac Injury.Journal of cellular and molecular medicine · 2026Article
- MG53 protects against intestinal inflammation by inhibiting NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- Exercise training for myocardial ischemia reperfusion injury: Mechanism and clinical practice (Review).International journal of molecular medicine · 2025Review
- Review
- Mitophagy in Hypertensive Cardiac Hypertrophy: Mechanisms and Therapeutic Implications.Journal of clinical hypertension (Greenwich, Conn.) · 2025Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischemic injury to the heart induces mitochondrial dysfunction due to increasing oxidative stress. MG53, also known as TRIM72, is highly expressed in striated muscle, is secreted as a myokine after exercise, and is essential for repairing damaged plasma membrane of many tissues by interacting with the membrane lipid phosphatidylserine (PS). We hypothesized MG53 could preserve mitochondrial integrity after an ischemic event by binding to the mitochondrial-specific lipid, cardiolipin (CL), for mitochondria protection to prevent mitophagy. Fluorescent imaging and Western blotting experiments showed recombinant human MG53 (rhMG53) translocated to the mitochondria after ischemic injury in vivo and in vitro. Fluorescent imaging indicated rhMG53 treatment reduced superoxide generation in ex vivo and in vitro models. Lipid-binding assay indicated MG53 binds to CL. Transfecting cardiomyocytes with the mitochondria-targeted mt-mKeima showed inhibition of mitophagy after MG53 treatment. Overall, we show that rhMG53 treatment may preserve cardiac function by preserving mitochondria in cardiomyocytes. These findings suggest MG53's interactions with mitochondria could be an attractive avenue for developing MG53 as a targeted protein therapy for cardioprotection.
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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.