Antioxidant Therapeutic Strategies for Cardiovascular Conditions Associated with Oxidative Stress

Abstract

Oxidative stress (OS) refers to the imbalance between the generation of reactive oxygen species (ROS) and the ability to scavenge these ROS by endogenous antioxidant systems, where ROS overwhelms the antioxidant capacity. Excessive presence of ROS results in irreversible damage to cell membranes, DNA, and other cellular structures by oxidizing lipids, proteins, and nucleic acids. Oxidative stress plays a crucial role in the pathogenesis of cardiovascular diseases related to hypoxia, cardiotoxicity and ischemia-reperfusion. Here, we describe the participation of OS in the pathophysiology of cardiovascular conditions such as myocardial infarction, anthracycline cardiotoxicity and congenital heart disease. This review focuses on the different clinical events where redox factors and OS are related to cardiovascular pathophysiology, giving to support for novel pharmacological therapies such as omega 3 fatty acids, non-selective betablockers and microRNAs.

Keywords: cardiac tissue; carvedilol; congenital heart disease; hypoxia; microRNA; omega 3 fatty acids; oxidative stress.

Figure 1

Representation of the cellular and molecular pathways of damage induced following a time course of hypoxia and ischemia–reperfusion cycle in different tissues. The activation of enzymatic and non-enzymatic sources of reactive oxygen species (ROS) is associated with the modulation of redox-sensitive transcriptional factors, such as the activation of nuclear factor (NF)-κB and inhibition of nuclear factor erythroid 2—related factor 2 (Nrf2). Both cellular pathways are implicated in the oxidative modifications or pro-inflammatory effects that can mediate structural or functional cardiovascular impairment.