ArticleJCI insight2018
Role of a TRIM72 ADP-ribosylation cycle in myocardial injury and membrane repair.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Post-translational modification-regulating biomaterials for regeneration.Bioactive materials · 2026Review
- The ADP-ribosyltransferases 3 (ART3) is a novel suppressor of pathological cardiac hypertrophy by ribosylating ITGA7.Acta pharmaceutica Sinica. B · 2026Article
- Metastasis-associated DNA methylation alterations persist after accounting for immune and stromal cell heterogeneity in primary colorectal tumors.Research square · 2026Article
- MLL1 promotes placental trophoblast ferroptosis and aggravates preeclampsia symptoms through epigenetic regulation of RBM15/TRIM72/ADAM9 axis.Biology direct · 2024Article
- ADP-ribose hydrolases: biological functions and potential therapeutic targets.Expert reviews in molecular medicine · 2024Review
- TRIM35 triggers cardiac remodeling by regulating SLC7A5-mediated amino acid transport and mTORC1 activation in fibroblasts.Cell communication and signaling : CCS · 2024Article
- Review
- Structural basis for TRIM72 oligomerization during membrane damage repair.Nature communications · 2023Article
- Blocking MG53Circulation research · 2022Article
- ARH Family of ADP-Ribose-Acceptor Hydrolases.Cells · 2022Review
- Review
- Review
- Effect of Parecoxib Sodium on Myocardial Ischemia-Reperfusion Injury Rats.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- TRIM72 promotes alveolar epithelial cell membrane repair and ameliorates lung fibrosis.Respiratory research · 2020Article
- The regulatory role of Myomaker and Myomixer-Myomerger-Minion in muscle development and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- ARH1 in Health and Disease.Cancers · 2020Review
- A knock-in mutation at cysteine 144 of TRIM72 is cardioprotective and reduces myocardial TRIM72 release.Journal of molecular and cellular cardiology · 2019Article
- Article
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Mono-ADP-ribosylation of an (arginine) protein catalyzed by ADP-ribosyltransferase 1 (ART1) - i.e., transfer of ADP-ribose from NAD to arginine - is reversed by ADP-ribosylarginine hydrolase 1 (ARH1) cleavage of the ADP-ribose-arginine bond. ARH1-deficient mice developed cardiomyopathy with myocardial fibrosis, decreased myocardial function under dobutamine stress, and increased susceptibility to ischemia/reperfusion injury. The membrane repair protein TRIM72 was identified as a substrate for ART1 and ARH1; ADP-ribosylated TRIM72 levels were greater in ARH1-deficient mice following ischemia/reperfusion injury. To understand better the role of TRIM72 and ADP-ribosylation, we used C2C12 myocytes. ARH1 knockdown in C2C12 myocytes increased ADP-ribosylation of TRIM72 and delayed wound healing in a scratch assay. Mutant TRIM72 (R207K, R260K) that is not ADP-ribosylated interfered with assembly of TRIM72 repair complexes at a site of laser-induced injury. The regulatory enzymes ART1 and ARH1 and their substrate TRIM72 were found in multiple complexes, which were coimmunoprecipitated from mouse heart lysates. In addition, the mono-ADP-ribosylation inhibitors vitamin K1 and novobiocin inhibited oligomerization of TRIM72, the mechanism by which TRIM72 is recruited to the site of injury. We propose that a mono-ADP-ribosylation cycle involving recruitment of TRIM72 and other regulatory factors to sites of membrane damage is critical for membrane repair and wound healing following myocardial injury.
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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.