Peroxiredoxin-5 Knockdown Accelerates Pressure Overload-Induced Cardiac Hypertrophy in Mice.

Chengyun Hu,Jianfeng Luo,Zhetao Zhang,Lai Jiang,Jie Gao,Fei Tang,Di Wang,Jun Huang,Feibiao Dai,Chaoliang Tang,Jiawu Wang,Ji Bihl

doi:10.1155/2022/5067544

Abstract

A recent study showed that peroxiredoxins (Prxs) play an important role in the development of pathological cardiac hypertrophy. However, the involvement of Prx5 in cardiac hypertrophy remains unclear. Therefore, this study is aimed at investigating the role and mechanisms of Prx5 in pathological cardiac hypertrophy and dysfunction. Transverse aortic constriction (TAC) surgery was performed to establish a pressure overload-induced cardiac hypertrophy model. In this study, we found that Prx5 expression was upregulated in hypertrophic hearts and cardiomyocytes. In addition, Prx5 knockdown accelerated pressure overload-induced cardiac hypertrophy and dysfunction in mice by activating oxidative stress and cardiomyocyte apoptosis. Importantly, heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) pathway activation. These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure.

Highlights

Pathological cardiac hypertrophy is a common pathophysiological process of various cardiovascular diseases, including hypertension, myocardial infarction, and heart failure [1,2,3]
Heart deterioration caused by Prx5 knockdown was related to mitogen-activated protein kinase (MAPK) activation
These findings suggest that Prx5 could be a novel target for treating cardiac hypertrophy and heart failure

Summary

Introduction

Pathological cardiac hypertrophy is a common pathophysiological process of various cardiovascular diseases, including hypertension, myocardial infarction, and heart failure [1,2,3]. It presents as thickening of the ventricular wall and decreased compliance of the ventricular wall [4,5,6]. Multiple mechanisms have been identified in the regulation of pathological cardiac hypertrophy, including oxidative stress, inflammation, autophagy, and cardiomyocyte apoptosis [7,8,9]. Many studies have shown that some family members of Prxs play an important role in the development of pathological cardiac hypertrophy [14, Oxidative Medicine and Cellular Longevity

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