ArticleJournal of molecular and cellular cardiology2017
MG53 is dispensable for T-tubule maturation but critical for maintaining T-tubule integrity following cardiac stress.
Article in Journal of molecular and cellular cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- MG53 protects against septic cardiac dysfunction by ubiquitinating ATF2.Journal of advanced research · 2026Article
- Matriglycan maintains t-tubule structural integrity in cardiac muscle.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Advances in the Study of MG53 in Cardiovascular Disease.International journal of general medicine · 2023Review
- Prohibiting MG53 Phosphorylation Optimizes its Therapeutic Potential in Diabetes.Circulation research · 2022Article
- Cardiac effects and clinical applications of MG53.Cell & bioscience · 2021Review
- Proteomic analysis identifies key differences in the cardiac interactomes of dystrophin and micro-dystrophin.Human molecular genetics · 2021Article
- Plasma membrane integrity: implications for health and disease.BMC biology · 2021Review
- The Pivotal Role of Mitsugumin 53 in Cardiovascular Diseases.Cardiovascular toxicology · 2021Review
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- LncRNA AK045171 protects the heart from cardiac hypertrophy by regulating the SP1/MG53 signalling pathway.Aging · 2020Article
- Cardiomyocyte damage control in heart failure and the role of the sarcolemma.Journal of muscle research and cell motility · 2019Article
- Cardiac Pathophysiology and the Future of Cardiac Therapies in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2019Review
- MG 53 Protein Protects Aortic Valve Interstitial Cells From Membrane Injury and Fibrocalcific Remodeling.Journal of the American Heart Association · 2019Article
- Automatic assessment of the cardiomyocyte development stages from confocal microscopy images using deep convolutional networks.PloS one · 2019Article
- MG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents.Communications biology · 2019Article
- Zinc in Wound Healing Modulation.Nutrients · 2017Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
The cardiac transverse (T)-tubule membrane system is the safeguard for cardiac function and undergoes dramatic remodeling in response to cardiac stress. However, the mechanism by which cardiomyocytes repair damaged T-tubule network remains unclear. In the present study, we tested the hypothesis that MG53, a muscle-specific membrane repair protein, antagonizes T-tubule damage to protect against maladaptive remodeling and thereby loss of excitation-contraction coupling and cardiac function. Using MG53-knockout (MG53-KO) mice, we first established that deficiency of MG53 had no impact on maturation of the T-tubule network in developing hearts. Additionally, MG53 ablation did not influence T-tubule integrity in unstressed adult hearts as late as 10months of age. Following left ventricular pressure overload-induced cardiac stress, MG53 protein levels were increased by approximately three-fold in wild-type mice, indicating that pathological stress induces a significant upregulation of MG53. MG53-deficient mice had worsened T-tubule disruption and pronounced dysregulation of Ca
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