Biomarkers of Oxidative Stress Tethered to Cardiovascular Diseases

Abstract

Cardiovascular disease (CVD) is a broad term that incorporated a group of conditions that affect the blood vessels and the heart. CVD is a foremost cause of fatalities around the world. Multiple pathophysiological mechanisms are involved in CVD; however, oxidative stress plays a vital role in generating reactive oxygen species (ROS). Oxidative stress occurs when the concentration of oxidants exceeds the potency of antioxidants within the body while producing reactive nitrogen species (RNS). ROS generated by oxidative stress disrupts cell signaling, DNA damage, lipids, and proteins, thereby resulting in inflammation and apoptosis. Mitochondria is the primary source of ROS production within cells. Increased ROS production reduces nitric oxide (NO) bioavailability, which elevates vasoconstriction within the arteries and contributes to the development of hypertension. ROS production has also been linked to the development of atherosclerotic plaque. Antioxidants can decrease oxidative stress in the body; however, various therapeutic drugs have been designed to treat oxidative stress damage due to CVD. The present review provides a detailed narrative of the oxidative stress and ROS generation with a primary focus on the oxidative stress biomarker and its association with CVD. We have also discussed the complex relationship between inflammation and endothelial dysfunction in CVD as well as oxidative stress-induced obesity in CVD. Finally, we discussed the role of antioxidants in reducing oxidative stress in CVD.

Low Level of Advanced Glycation End Products in Serum of Patients with Allergic Rhinitis and Chronic Epstein-Barr Virus Infection at Different Stages of Virus Persistence

“…Besides ROI, reactive nitrogen species (RNS) are involved in tissue destruction, forming nitrotyrosine, a product of tyrosine nitration mediated by reactive nitrogen species such as peroxynitrite anion and nitrogen dioxide. Nitrotyrosine is identified as an indicator or marker of cell damage, inflammation, and NO (nitric oxide) production [49].…”

Perspectives on the Molecular Mediators of Oxidative Stress and Antioxidant Strategies in the Context of Neuroprotection and Neurolongevity: An Extensive Review

“…There are numerous methods and assays that may be used to determine the status of the OxS biomarkers in a range of biological samples, which is a major advantage but also a downside. Each method has its own set of pros and limitations, as well as practicality and economic considerations [158]. The interpretation of data may also be complicated by a number of pre-and post-analytical difficulties, which require further standardization such as preanalytical issues, analytical issues and, postanalytical issues [159].…”

Advances in the study of nicotinamide adenine dinucleotide phosphate oxidase in myocardial remodeling

“…However, excess ROS can cause redox imbalance, resulting in myocardial cell apoptosis and necrosis, fibroblast proliferation, activation of matrix metalloproteinases (MMPs), collagen deposition, and other pathophysiological processes, activating oxidative stress and causing pathological myocardial remodeling, leading to various diseases, such as myocardial infarction, hypertension, arrhythmia, heart failure, and vascular dysfunction ( 21 – 23 ). Excessive production of ROS also activates a variety of hypertrophic signaling kinases and transcription factors, disrupting the contractile function of excitation-contraction coupling core proteins, causing mitochondrial DNA(mtDNA) damage, lipid and protein peroxidation, abnormal ion channel function, leading to fibroblast proliferation, vascular endothelial dysfunction, interstitial fibrosis, atheromatous plaque formation, thromboembolism formation and inadequate cardiac energy supply, eventually progressing to heart failure ( 24 – 28 ). Recent studies have shown that ROS produced by mitochondria activate the oxidative stress process, causing apoptosis and interstitial fibrosis, resulting in functional and structural impairment, leading to deterioration of right ventricular (RV) function and pressure overload, which in turn leads to right heart failure ( 29 ).…”