ArticleThe Journal of clinical investigation2020
Autoantibodies targeting TRIM72 compromise membrane repair and contribute to inflammatory myopathy.
Article in The Journal of clinical investigation, 2020. 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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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.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- Roles and Mechanisms of TRIM Family Proteins in Inflammation in the Brain and Beyond.International journal of molecular sciences · 2026Review
- MG53 protects against septic cardiac dysfunction by ubiquitinating ATF2.Journal of advanced research · 2026Article
- Recent advances in immunological mechanisms and murine disease models of idiopathic inflammatory myopathies.Inflammation and regeneration · 2025Review
- Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies.medRxiv : the preprint server for health sciences · 2025Article
- Plasma membrane repair defect in Alzheimer's disease neurons is driven by the reduced dysferlin expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Mitochondria-encoded peptide MOTS-c participates in plasma membrane repair by facilitating the translocation of TRIM72 to membrane.Theranostics · 2024Article
- Pathogenic mechanisms of disease in idiopathic inflammatory myopathies: autoantibodies as clues.Frontiers in immunology · 2024Review
- Role of calcium-sensor proteins in cell membrane repair.Bioscience reports · 2023Review
- Genetic Influences in Cancer-Associated Myositis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
- TRIM72 Alleviates Muscle Inflammation in mdx Mice via Promoting Mitophagy-Mediated NLRP3 Inflammasome Inactivation.Oxidative medicine and cellular longevity · 2023Article
- The cell membrane repair protein MG53 modulates transcription factor NF-κB signaling to control kidney fibrosis.Kidney international · 2022Article
- TRIMs: selective recruitment at different steps of the NF-κB pathway-determinant of activation or resolution of inflammation.Cellular and molecular life sciences : CMLS · 2021Review
- Plasma membrane integrity in health and disease: significance and therapeutic potential.Cell discovery · 2021Review
- Neuromuscular disease: 2021 update.Free neuropathology · 2021Article
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14 authors at 2 institutions in 1 country.
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Abstract
Idiopathic inflammatory myopathies (IIM) involve chronic inflammation of skeletal muscle and subsequent muscle degeneration due to an uncontrolled autoimmune response; however, the mechanisms leading to pathogenesis are not well understood. A compromised sarcolemmal repair process could promote an aberrant exposure of intramuscular antigens with the subsequent initiation of an inflammatory response that contributes to IIM. Using an adoptive transfer mouse model of IIM, we show that sarcolemmal repair is significantly compromised in distal skeletal muscle in the absence of inflammation. We identified autoantibodies against TRIM72 (also known as MG53), a muscle-enriched membrane repair protein, in IIM patient sera and in our mouse model of IIM by ELISA. We found that patient sera with elevated levels of TRIM72 autoantibodies suppress sarcolemmal resealing in healthy skeletal muscle, and depletion of TRIM72 antibodies from these same serum samples rescues sarcolemmal repair capacity. Autoantibodies targeting TRIM72 lead to skeletal muscle fibers with compromised membrane barrier function, providing a continuous source of autoantigens to promote autoimmunity and further amplifying humoral responses. These findings reveal a potential pathogenic mechanism that acts as a feedback loop contributing to the progression of IIM.
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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.