Telmisartan suppresses cardiomyocyte and alveolar wall hypertrophy by the PPARγ-ERK-NFAT complex by changing the balance of PPARγ and ERK.
Year: 2019
Type: article
Abstract: with increased pathologic protein synthesis and NFAT nuclear translocation. Telmisartan suppressed angiotensin II-induced cardiomyocyte hypertrophy by inhibiting protein synthesis and NFAT nuclear translocation. The inhibition by telmisartan was reversed by both a PPARγ inhibitor and ERK activator. These results indicated that PPARγ and ERK play opposing roles in regulating telmisartan inhibition of cardiomyocyte hypertrophy. When we precipitated cardiomyocyte NFAT, we found that PPARγ and ERK bind to NFAT, indicating that the PPARγ-ERK-NFAT complex mediated telmisartan inhibition of cardiomyocyte hypertrophy. In this complex, the balance of PPARγ and ERK is critical to regulate NFAT function. Finally, we created a new model to explain the mechanism by which telmisartan prevents cardiomyocyte hypertrophy.
Source: PubMed Central
Authors: Chenguang Ma, Yang Pu, Hua Xue, Yang Liu
Institution: Heilongjiang Provincial Hospital
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W3007519412