1. Sodium butyrate alleviates right ventricular hypertrophy in pulmonary arterial hypertension by inhibiting H19 and affecting the activation of let-7g-5p/IGF1 receptor/ERK.
- Author
-
Li, Ming-hui, Liu, Xu, Xie, Yu-liang, Tang, Xiao-guang, Song, Liao-fan, Zhao, Fan-rong, Chen, Yu-jing, Guo, Chao, Zhang, Wei-fang, and Zhu, Tian-tian
- Subjects
- *
RIGHT ventricular hypertrophy , *PULMONARY arterial hypertension , *SODIUM butyrate , *BONE morphogenetic protein receptors , *SOMATOMEDIN C , *CARDIAC hypertrophy , *ENDOTHELIN receptors , *INSULIN-like growth factor receptors - Abstract
Pulmonary arterial hypertension (PAH) is a complex and fatal cardio-pulmonary vascular disease. Decompensated right ventricular hypertrophy (RVH) caused by cardiomyocyte hypertrophy often leads to fatal heart failure, the leading cause of mortality among patients. Sodium butyrate (SB), a compound known to reduce cardiac hypertrophy, was examined for its potential effect and the underlying mechanism of SB on PAH-RVH. The in vivo study showed that SB alleviated RVH and cardiac dysfunction, as well as improved life span and survival rate in MCT-PAH rats. The in vivo and in vitro experiments showed that SB could attenuate cardiomyocyte hypertrophy by reversing the expressions of H19, let-7g-5p, insulin-like growth factor 1 receptor (IGF1 receptor), and p ERK. H19 inhibition restored the level of let-7g-5p and prevented the overexpression of IGF1 receptor and p ERK in hypertrophic cardiomyocytes. In addition, dual luciferase assay revealed that H19 demonstrated significant binding with let-7g-5p, acting as its endogenous RNA. Briefly, SB attenuated PAH-RVH by inhibiting the H19 overexpression, restoring the level of let-7g-5p, and hindering IGF1 receptor/ERK activation. [Display omitted] [ABSTRACT FROM AUTHOR]
- Published
- 2024
- Full Text
- View/download PDF