ArticleDiabetes2022
MG53 E3 Ligase-Dead Mutant Protects Diabetic Hearts From Acute Ischemic/Reperfusion Injury and Ameliorates Diet-Induced Cardiometabolic Damage.
Article in Diabetes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- MG53 protects against septic cardiac dysfunction by ubiquitinating ATF2.Journal of advanced research · 2026Article
- Myocardial Infarction in Murine Models of Obesity and Related Metabolic Disorders: The Role of Inflammation.International journal of molecular sciences · 2025Review
- Review
- MuRF1 Partners With TRIM72 to Impair Insulin Signaling in Skeletal Muscle Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Liver X Receptor Activation Alleviates Hepatic Ischemia-Reperfusion Injury in Diabetes by Inhibiting NF-κB-NLRP3 Activation.Immunity, inflammation and disease · 2025Article
- Mitsugumin 53 drives stem cell differentiation easing intestinal injury and inflammation.Signal transduction and targeted therapy · 2025Article
- Ubiquitination in diabetes and its complications: A perspective from bibliometrics.World journal of diabetes · 2025Article
- Circulating Myokines as Novel Biomarkers for Cardiovascular Diseases.Reviews in cardiovascular medicine · 2024Review
- Mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to membrane.Theranostics · 2024Article
- E3 ligase MG53 suppresses tumor growth by degrading cyclin D1.Signal transduction and targeted therapy · 2023Article
- Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice.Biomedicines · 2023Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
- Prohibiting MG53 Phosphorylation Optimizes its Therapeutic Potential in Diabetes.Circulation research · 2022Article
- Blocking MG53Circulation research · 2022Article
- MG53 preserves mitochondrial integrity of cardiomyocytes during ischemia reperfusion-induced oxidative stress.Redox biology · 2022Article
- TRIM21 aggravates cardiac injury after myocardial infarction by promoting M1 macrophage polarization.Frontiers in immunology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiometabolic diseases, including diabetes and its cardiovascular complications, are the global leading causes of death, highlighting a major unmet medical need. Over the past decade, mitsugumin 53 (MG53), also called TRIM72, has emerged as a powerful agent for myocardial membrane repair and cardioprotection, but its therapeutic value is complicated by its E3 ligase activity, which mediates metabolic disorders. Here, we show that an E3 ligase-dead mutant, MG53-C14A, retains its cardioprotective function without causing metabolic adverse effects. When administered in normal animals, both the recombinant human wild-type MG53 protein (rhMG53-WT) and its E3 ligase-dead mutant (rhMG53-C14A) protected the heart equally from myocardial infarction and ischemia/reperfusion (I/R) injury. However, in diabetic db/db mice, rhMG53-WT treatment markedly aggravated hyperglycemia, cardiac I/R injury, and mortality, whereas acute and chronic treatment with rhMG53-C14A still effectively ameliorated I/R-induced myocardial injury and mortality or diabetic cardiomyopathy, respectively, without metabolic adverse effects. Furthermore, knock-in of MG53-C14A protected the mice from high-fat diet-induced metabolic disorders and cardiac damage. Thus, the E3 ligase-dead mutant MG53-C14A not only protects the heart from acute myocardial injury but also counteracts metabolic stress, providing a potentially important therapy for the treatment of acute myocardial injury in metabolic disorders, including diabetes and obesity.
Indexed as
Identifiers
What OpenQuestion holds
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.