ArticleJACC. Basic to translational science2024
TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway.
Article in JACC. Basic to translational science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Cardiac-targeted delivery of miRNA via antioxidant nanozymes ameliorates cardiac dysfunction and fibrosis after myocardial infarction.Journal of nanobiotechnology · 2026Article
- Identification of PANoptosis-related hub genes in acute myocardial infarction: diagnostic potential, immune correlates, and therapeutic insights.Journal of cardiothoracic surgery · 2026Article
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Article
- Article
- Machine Learning Integrates Bulk and Single-Nucleus RNA Sequence to Explore Apoptosis-Related Gene in Myocardial Infarction.Cardiovascular therapeutics · 2026Article
- Breakthroughs of ultrasound-targeted microbubble destruction in treating myocardial ischemia-reperfusion injury: from angiogenesis regulation to precise inflammation suppression.Drug delivery · 2025Review
- Acute Myocardial Infarction: Molecular Pathogenesis, Diagnosis, and Clinical Management.MedComm · 2025Review
- TRIM55: An Enemy at the Post-MI Border?: TRIMming May Not Always Be Good.JACC. Basic to translational science · 2024Article
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Authors and funding
11 authors.
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Abstract
Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro. The results showed that Trim55 knockout improved cardiac function and apoptosis after myocardial infarction, and overexpression aggravated cardiac function damage. The mechanism is that Trim55 interacts with nuclear factor, erythroid derived 2 (Nrf2) to accelerate its degradation and inhibit the expression of heme oxygenase 1, thereby promoting cardiomyocyte apoptosis.
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