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.

Highlights

  • Hypoxia-related cardiovascular pathologies, such as myocardial infarction, stroke, peripheral vascular disease and renal ischemia, are among the most frequent causes of death and disability [1].Hypoxia is defined as the threshold where the oxygen concentration is a limiting factor for normal cellular processes, including ATP synthesis

  • The antineoplastic mechanisms of action of these chemotherapeutics agents are multiple, they have in common the induction of oxidative stress in non-target tissues, thereby leading to “normal tissue injury” [140], which occurs for example with cyclophosphamide, cisplatin, busulfan, mitomycin, fluorouracil, cytarabine, and bleomycin [140].Among these agents, 5-fluorouracil and its prodrug capecitabine are some of the most important agents because they are the most common causes of chemotherapy-related cardiotoxicity after the anthracyclines, and depending on the study, its rates of toxicity range from 1 to 19% [141]

  • A continuously growing body of evidence shows that Oxidative stress (OS) seems to be of key importance in the pathogenesis of several types of cardiovascular diseases

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Summary

Introduction

Hypoxia-related cardiovascular pathologies, such as myocardial infarction, stroke, peripheral vascular disease and renal ischemia, are among the most frequent causes of death and disability [1]. Hypoxia is defined as the threshold where the oxygen concentration is a limiting factor for normal cellular processes, including ATP synthesis. Nutrients 2017, 9, 966 process fails, a prolonged inadequate vascular supply of oxygen leads to chronic hypoxia and can cause chronic diseases. Some cardiovascular diseases are related to the re-exposure to physiologic or supra-normal oxygen concentrations after a hypoxic insult, which constitute the basis for ischemia–reperfusion injury. Oxidative stress (OS) seems to be a common pathway in several morbid states in which myocardial injury is the primary determinant. The involvement of oxidative stress in cardiovascular disease is explored and redox-based strategies are reviewed in representative conditions that serve as prototypical models for antioxidant therapies development

Oxidative Stress in Cardiovascular Disease
Cardiac Ischemic Preconditioning
Pharmacological Preconditioning
Cardiac Preconditioning with Omega 3
Antioxidant Mechanism Induced by Omega 3
Oxidative Stress and Cardiotoxicity
Mechanisms of Anthracycline-Induced Cardiotoxicity
Reactive Oxygen Species Scavengers
Prevention of Reactive Oxygen Species Generation
Chemotherapy-Induced Cardiotoxicity of Other Non-Anthracycline Agents
Results
Antioxidant-Based Strategies in Congenital Heart Disease Surgical Correction
Antioxidants
Controlling Oxygen Supply
Propofol Anesthesia
Novel Experimental Antioxidant-Based Therapies
Concluding Remarks
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