ArticleActa pharmacologica Sinica2020
MG53 protects against contrast-induced acute kidney injury by reducing cell membrane damage and apoptosis.
Article in Acta pharmacologica Sinica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 27 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
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Machine learning-guided Nano-QSAR modeling predicts HepaRG cell membrane toxicity of engineered nanoparticles with mechanistic insights.Cell biology and toxicology · 2026Article
- MG53 protects against intestinal inflammation by inhibiting NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- Mitochondrial DNA methylation is involved in contrast-induced renal tubular epithelial cell injury.Renal failure · 2025Article
- Treatment with MG53 ameliorates traumatic brain injury-associated acute kidney injury.The journal of trauma and acute care surgery · 2025Article
- Mitsugumin 53 Inhibits Angiogenesis Through Regulating Focal Adhesion Turnover and Tip Cell Formation.Journal of cellular and molecular medicine · 2025Article
- Recombinant human mitsugumin 53: a potential therapeutic agent for multiple diseases.Frontiers in pharmacology · 2025Review
- The Potential Role of Cardiokines in Heart and Kidney Diseases.Current medicinal chemistry · 2025Review
- Association Between Lower Serum Mitsugumin 53 Levels and the Risk of Vascular Calcification in Hemodialysis Patients.International journal of nephrology and renovascular disease · 2025Article
- Trim72 is a major host factor protecting against lethal Candida albicans infection.PLoS pathogens · 2024Article
- Multipronged regulation of autophagy and apoptosis: emerging role of TRIM proteins.Cellular & molecular biology letters · 2024Review
- MG53/TRIM72: multi-organ repair protein and beyond.Frontiers in physiology · 2024Review
- Review
- Structural basis for TRIM72 oligomerization during membrane damage repair.Nature communications · 2023Article
- MG53: A potential therapeutic target for kidney disease.Pharmacology research & perspectives · 2023Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
- Arctigenin attenuates paraquat-induced human lung epithelial A549 cell injury by suppressing ROS/p38 mitogen-activated protein kinases-mediated apoptosis.World journal of emergency medicine · 2022Article
- Muscle multiorgan crosstalk with MG53 as a myokine for tissue repair and regeneration.Current opinion in pharmacology · 2021Review
- Increased ATHypertension research : official journal of the Japanese Society of Hypertension · 2021Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
Abstract
Mitsugumin 53 (MG53) is a tripartite motif family protein that has been reported to attenuate injury via membrane repair in different organs. Contrast-induced acute kidney injury (CI-AKI) is a common complication caused by the administration of iodinated contrast media (CM). While the cytotoxicity induced by CM leading to tubular cell death may be initiated by cell membrane damage, we wondered whether MG53 alleviates CI-AKI. This study was designed to investigate the effect of MG53 on CI-AKI and the underlying mechanism. A rat model of CI-AKI was established, and CI-AKI induced the translocation of MG53 from serum to injury sites on the renal proximal tubular (RPT) epithelia, as illustrated by immunoblot analysis and immunohistochemical staining. Moreover, pretreatment of rats with recombinant human MG53 protein (rhMG53, 2 mg/mL) alleviated iopromide-induced injury in the kidney, which was determined by measuring serum creatinine, blood urea nitrogen and renal histological changes. In vitro studies demonstrated that exposure of RPT cells to iopromide (20, 40, and 80 mg/mL) caused cell membrane injury and cell death, which were attenuated by rhMG53 (10 and 50 μg/mL). Mechanistically, MG53 translocated to the injury site on RPT cells and bound to phosphatidylserine to protect RPT cells from iopromide-induced injury. In conclusion, MG53 protects against CI-AKI through cell membrane repair and reducing cell apoptosis; therefore, rhMG53 might be a potential effective means to treat or prevent CI-AKI.
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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.