ArticleKidney international2022
The cell membrane repair protein MG53 modulates transcription factor NF-κB signaling to control kidney fibrosis.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- The Heart-Kidney Axis in Heart Failure and Chronic Kidney Disease: Mechanisms, Mediators, and Therapeutic Implications.Biomolecules · 2026Review
- Pro-inflammatory cytokine IFN-γ protects against renal fibrosis by promoting E3 ubiquitin ligase Trim21-mediated Loxl2 degradation in tubular epithelial cells.Cell death & disease · 2026Article
- NINJ1 ubiquitination by TRIM72 protects against plasma membrane rupture and AKI-CKD progression.Cell death and differentiation · 2026Article
- 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
- MG53 protects against septic cardiac dysfunction by ubiquitinating ATF2.Journal of advanced research · 2026Article
- XBP1s-Orchestrated Soluble Mediators: Participants of Oxidative Stress in Renal Ischemia-Reperfusion Injury Following Donation After Circulatory Death.Mediators of inflammation · 2026Review
- Multi-omics and machine learning reveal LYZ and ISG15 as diagnostic and therapeutic targets in autoimmune-mediated chronic kidney disease.Frontiers in immunology · 2026Article
- MG53 protects against intestinal inflammation by inhibiting NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- Tanshinone IIA reduces tubulointerstitial fibrosis by suppressing GSDMD-mediated pyroptosis.Pharmaceutical biology · 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
- Current Perspectives on the NF-κB Signaling Axis as a Potential Pharmacological Target in Cardiorenal Syndrome.Drug design, development and therapy · 2025Review
- Pulsed radiofrequency alleviates neuropathic pain by upregulating MG53 to inhibit microglial activation.European journal of medical research · 2024Article
- Rodent models of AKI and AKI-CKD transition: an update in 2024.American journal of physiology. Renal physiology · 2024Review
- The E3 ubiquitin ligase TRIM39 modulates renal fibrosis induced by unilateral ureteral obstruction through regulating proteasomal degradation of PRDX3.Cell death discovery · 2024Article
- Diosmin ameliorates renal fibrosis through inhibition of inflammation by regulating SIRT3-mediated NF-κB p65 nuclear translocation.BMC complementary medicine and therapies · 2024Article
- HDAC9 as a Privileged Target: Reviewing its Role in Different Diseases and Structure-activity Relationships (SARs) of its Inhibitors.Mini reviews in medicinal chemistry · 2024Review
- HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice.Nature communications · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Kidney fibrosis is associated with the progression of acute kidney injury to chronic kidney disease. MG53, a cell membrane repair protein, has been shown to protect against injury to kidney epithelial cells and acute kidney injury. Here, we evaluated the role of MG53 in modulation of kidney fibrosis in aging mice and in mice with unilateral ureteral obstruction (UUO) a known model of progressive kidney fibrosis. Mice with ablation of MG53 developed more interstitial fibrosis with age than MG53-intact mice of the same age. Similarly, in the absence of MG53, kidney fibrosis was exaggerated compared to mice with intact MG53 in the obstructed kidney compared to the contralateral unobstructed kidney or the kidneys of sham operated mice. The ureteral obstructed kidneys from MG53 deficient mice also showed significantly more inflammation than ureteral obstructed kidneys from MG53 intact mice. In vitro experiments demonstrated that MG53 could enter the nuclei of proximal tubular epithelial cells and directly interact with the p65 component of transcription factor NF-κB, providing a possible explanation of enhanced inflammation in the absence of MG53. To test this, enhanced MG53 expression through engineered cells or direct recombinant protein delivery was given to mice subject to UUO. This reduced NF-κB activation and inflammation and attenuated kidney fibrosis. Thus, MG53 may have a therapeutic role in treating chronic kidney inflammation and thereby provide protection against fibrosis that leads to the chronic kidney disease phenotype.
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