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微小RNA-133b-3p通过靶向抑制凋亡减轻血管紧张素II诱导的心肌肥大。

MiR-133b-3p attenuates angiotensin II-induced cardiac hypertrophy through the inhibition of apoptosis by targeting .

作者信息

Gu Jiwei, Li Zhen, Li Xinyi, Yang Ziyao, Xu Xi, Wang Yanjia, Li Xiaohan, Qin Kaiyue, Li Guizhong, Xue Li, Yang Xiaoling

机构信息

NHC Key Laboratory of Metabolic Cardiovascular Diseases Research, Ningxia Medical University, Yinchuan 750004, China.

Department of Cardiovascular Surgery, General Hospital of Ningxia Medical University, Yinchuan 750004, China.

出版信息

Acta Biochim Biophys Sin (Shanghai). 2025 Feb 12;57(6):916-926. doi: 10.3724/abbs.2024181.

Abstract

MicroRNAs (miRNAs) have emerged as essential regulators that play important roles in the development of multiple systems. Recent studies have identified significant roles for miRNAs in the progression of cardiac hypertrophy. This study aims to investigate the effects of miR-133b-3p on angiotensin II (Ang II)-induced cardiac hypertrophy and apoptosis, as well as explore its underlying mechanisms. Our experimental results reveal that miR-133b-3p expression is significantly decreased in both animal and cell models of cardiac hypertrophy induced by Ang II. Overexpression of miR-133b-3p reverses the hypertrophic manifestations and apoptosis induced by Ang II. Through bioinformatics analysis and dual-luciferase reporter assays, (cell death inducing p53 target 1) is identified as a direct target of miR-133b-3p, and the overexpression of miR-133b-3p reduces expression. Additionally, silencing suppresses cardiomyocyte hypertrophy and apoptosis induced by Ang II. In summary, these results suggest that miR-133b-3p may serve as a potential diagnostic marker for cardiac hypertrophy and that the upregulation of miR-133b-3p inhibits cardiac hypertrophy by targeting .

摘要

微小RNA(miRNA)已成为重要的调节因子,在多个系统的发育中发挥重要作用。最近的研究已经确定miRNA在心肌肥大进展中具有重要作用。本研究旨在探讨miR-133b-3p对血管紧张素II(Ang II)诱导的心肌肥大和细胞凋亡的影响,并探索其潜在机制。我们的实验结果表明,在Ang II诱导的心肌肥大动物模型和细胞模型中,miR-133b-3p的表达均显著降低。miR-133b-3p的过表达可逆转Ang II诱导的肥大表现和细胞凋亡。通过生物信息学分析和双荧光素酶报告基因检测,(细胞死亡诱导p53靶点1)被确定为miR-133b-3p的直接靶点,miR-133b-3p的过表达降低了其表达。此外,的沉默可抑制Ang II诱导的心肌细胞肥大和细胞凋亡。总之,这些结果表明,miR-133b-3p可能作为心肌肥大的潜在诊断标志物,并且miR-133b-3p的上调通过靶向抑制心肌肥大。

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