| First Author | Hou H | Year | 2023 |
| Journal | Mol Med Rep | Volume | 28 |
| Issue | 3 | PubMed ID | 37503784 |
| Mgi Jnum | J:340097 | Mgi Id | MGI:7525776 |
| Doi | 10.3892/mmr.2023.13060 | Citation | Hou H, et al. (2023) Tripartite motifcontaining 14 may aggravate cardiac hypertrophy via the AKT signalling pathway in neonatal rat cardiomyocytes and transgenic mice. Mol Med Rep 28(3) |
| abstractText | Tripartite motifcontaining 14 (TRIM14) is an E3 ubiquitin ligase that primarily participates in the natural immune response and in tumour development via ubiquitination. However, the role of TRIM14 in cardiac hypertrophy is not currently clear. The present study examined the role of TRIM14 in cardiac hypertrophy and its potential molecular mechanism. TRIM14 was overexpressed in neonatal rat cardiomyocytes using adenovirus and cardiomyocyte hypertrophy was induced using phenylephrine (PE). Cardiomyocyte hypertrophy was assessed by measuring cardiomyocyte surface area and markers of hypertrophy. In addition, TRIM14transgenic (TRIM14TG) mice were created and cardiac hypertrophy was induced using transverse aortic constriction (TAC). Cardiac function, heart weighttobody weight ratio (HW/BW), cardiomyocyte crosssectional area, cardiac fibrosis and hypertrophic markers were further examined. The expression of AKT signalling pathwayrelated proteins was detected. TRIM14 overexpression in cardiomyocytes promoted PEinduced increases in cardiomyocyte surface area and hypertrophic markers. TRIM14TG mice developed worse cardiac function, greater HW/BW, crosssectional area and cardiac fibrosis, and higher levels of hypertrophic markers in response to TAC. TRIM14 overexpression also increased the phosphorylation levels of AKT, GSK3beta, mTOR and p70S6K in vivo and in vitro. To the best our knowledge, the present study was the first to reveal that overexpression of TRIM14 aggravated cardiac hypertrophy in vivo and in vitro, which may be related to activation of the AKT signalling pathway. |
