Author:
Jeong Se-Jin,Park Jong-Gil,Oh Goo Taeg
Abstract
Increased oxidative stress (OS) is considered a common etiology in the pathogenesis of cardiovascular disease (CVD). Therefore, the precise regulation of reactive oxygen species (ROS) in cardiovascular cells is essential to maintain normal physiological functions. Numerous regulators of cellular homeostasis are reportedly influenced by ROS. Hydrogen peroxide (H2O2), as an endogenous ROS in aerobic cells, is a toxic substance that can induce OS. However, many studies conducted over the past two decades have provided substantial evidence that H2O2 acts as a diffusible intracellular signaling messenger. Antioxidant enzymes, including superoxide dismutases, catalase, glutathione peroxidases, and peroxiredoxins (Prdxs), maintain the balance of ROS levels against augmentation of ROS production during the pathogenesis of CVD. Especially, Prdxs are regulatory sensors of transduced intracellular signals. The intracellular abundance of Prdxs that specifically react with H2O2 act as regulatory proteins. In this review, we focus on the role of Prdxs in the regulation of ROS-induced pathological changes in the development of CVD.
Funder
National Research Foundation of Korea
Korea Research Institute of Bioscience and Biotechnology
Subject
Cell Biology,Clinical Biochemistry,Molecular Biology,Biochemistry,Physiology
Reference124 articles.
1. Oxidative stress and heart failure
2. Oxidative stress and hypertension: Possibility of hypertension therapy with antioxidants;Baradaran;J. Res. Med. Sci.,2014
3. Oxidative Stress in Atherosclerosis
4. Redefining Oxidative Stress
5. CVD and Oxidative Stress
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