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.

Oxidative Stress-Responsive MicroRNAs in Heart Injury

“…Several studies demonstrated that cardiac hypertrophy is caused by switching of adult alpha myosin heavy chain (α-MHC, known as Myh6) to fetal beta myosin heavy chain (β-MHC, known as Myh7) gene expression. In experimental studies, deletion of miRNA-208a, which is encoded in the intron of the Myh6 gene, leads to the decreased expression of the Myh7 gene in response to stress and to hypertrophy [88,98]. These results were confirmed in the study of Rawal et al, where inhibition of miRNA-208a hampers the activation of β-MHC and hypertrophic response [99].…”

“…Oxidative stress plays a crucial role in many cardiovascular diseases, like hypoxia, ischemia/reperfusion injury, or heart failure [88]. As mentioned before, intracellular ROS are formed in normal conditions as the result of normal mitochondrial respiration, but ROS are also produced during reperfusion in hypoxic tissue and in association with infection and inflammation, leading to pathological conditions of the heart [88,89]. One of the effects of ROS accumulation in cardiomyocytes is a different expression of noncoding RNAs (ncRNAs), subsequently contributing to cell apoptosis and heart pathology.…”

Level of Certain Oxidants and Antioxidants in Patients with Uterine Fibroids

“…The control of oxidative stress caused by these reasons is thought to be effective in the prophylaxis of uterine fibroids. Nowadays, it is known that antioxidant agents and related diet products contribute to the process and have a role in treatment in many pathological conditions (36)(37)(38). Considering all these mechanisms, the role of antioxidant agents in the treatment of uterine fibroids can be discussed.…”

Protective effects of S‐carvedilol on doxorubicin‐induced damages to human umbilical vein endothelial cells and rats

“…CAR is a third‐generation neurohormonal antagonist with multiple activities and it blocks both α‐, β 1 ‐ and β 2 ‐adrenergic receptors. In addition to its well‐known properties, CAR has a number of ancillary activities, including antioxidant (Farías et al, ; Areti, Komirishetty, & Kumar, ), anti‐inflammatory and anti‐apoptotic properties, and appears to reduce DOX cardiotoxicity (Matsui et al, ; Santos, Moreno, Leino, Froberg, & Wallace, ). The antioxidant activity of CAR has been widely implicated in enhancing the free radical‐mediated toxicity caused by DOX, diminishing the DOX‐induced negative impact on systolic blood pressure (BP) and left ventricular fractional shortening (Fazio et al, ), and on increased lipid peroxidation (Matsui et al, ; Oliveira et al, ).…”