ArticleBioengineered2022
Tripartite motif 27 promotes cardiac hypertrophy via PTEN/Akt/mTOR signal pathways.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 11 citations in OpenAlex.
- CRISPR screening identifies TRIM27 as a destabilizer of the Smith-Magenis syndrome protein RAI1.Genetics · 2026Article
- Review
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Exploring Phosphatase and Tensin Homologue Deleted on Chromosome Ten (PTEN) as a Potential Therapeutic Target for Cardiac Hypertrophy.ACS pharmacology & translational science · 2025Review
- Unraveling the heart-brain axis: shared genetic mechanisms in cardiovascular diseases and Schizophrenia.Schizophrenia (Heidelberg, Germany) · 2024Article
- TRIM27 Promotes Endothelial Progenitor Cell Apoptosis in Patients with In-Stent Restenosis by Ubiquitinating TBK1.Applied biochemistry and biotechnology · 2024Article
- Intricate confrontation: Research progress and application potential of TRIM family proteins in tumor immune escape.Journal of advanced research · 2023Review
- Tripartite motif‑containing 14 may aggravate cardiac hypertrophy via the AKT signalling pathway in neonatal rat cardiomyocytes and transgenic mice.Molecular medicine reports · 2023Article
- AKT-mTOR signaling-mediated rescue ofCardiovascular diagnosis and therapy · 2022Article
- Hsp72-Based Effect and Mechanism of Microwave Radiation-Induced Cardiac Injury in Rats.Oxidative medicine and cellular longevity · 2022Article
- TRIM27 is an adverse prognostic biomarker and associated with immune and molecular profiles in right-sided colon cancer.American journal of cancer research · 2022Article
- Emerging roles of TRIM27 in cancer and other human diseases.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tripartite motif-containing 27 (Trim27) is highly expressed in tumor cells and regulates natural immunity and apoptosis. However, the effects of Trim27 in cardiac hypertrophy are not fully elucidated. In this study, we tried to explore the potential role of Trim27 in pressure overload-induced cardiac hypertrophy and the underlying mechanism. The results indicated that compared to sham operation (Sham) group, transverse aortic constriction (TAC) group showed significantly up-regulated Trim27 protein expression (P < 0.05). The neonatal rat cardiomyocytes (NRCMs) were isolated and stimulated with PBS, angiotensin (AngII) and phenylephrine (PE). NRCMs were collected to detect the protein expression of Trim27. The results were consistent with the results in vivo. Compared to PBS treatment, the expression of Trim27 protein in NRCMs was significantly increased after PE or AngII stimulation (P < 0.05, respectively). Knockout of Trim27 can reduce the size of cardiomyocytes and reduce the proteins expression of ANP, BNP, and β-MHC, improve cardiac function, and reverse myocardial hypertrophy (P < 0.05). Trim27 may be involved in regulating the development of cardiac hypertrophy. Further results showed that Trim27 can increase the protein expression of phosphorylation of Akt, GSK3β, mTOR, and P70s6k by interacting with PTEN (phosphatase tensin homolog). These findings revealed that Trim27 can promote cardiac hypertrophy by activating PTEN/Akt/GSK3β/mTOR signaling pathway.
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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 Socratic graph.