Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease

Abstract

Cardiovascular diseases (CVDs) continue to exert a significant impact on global mortality rates, encompassing conditions like pulmonary arterial hypertension (PAH), atherosclerosis (AS), and myocardial infarction (MI). Oxidative stress (OS) plays a crucial role in the pathogenesis and advancement of CVDs, highlighting its significance as a contributing factor. Maintaining an equilibrium between reactive oxygen species (ROS) and antioxidant systems not only aids in mitigating oxidative stress but also confers protective benefits on cardiac health. Herbal monomers can inhibit OS in CVDs by activating multiple signaling pathways, such as increasing the activity of endogenous antioxidant systems and decreasing the level of ROS expression. Given the actions of herbal monomers to significantly protect the normal function of the heart and reduce the damage caused by OS to the organism. Hence, it is imperative to recognize the significance of herbal monomers as prospective therapeutic interventions for mitigating oxidative damage in CVDs. This paper aims to comprehensively review the origins and mechanisms underlying OS, elucidate the intricate association between CVDs and OS, and explore the therapeutic potential of antioxidant treatment utilizing herbal monomers. Furthermore, particular emphasis will be placed on examining the cardioprotective effects of herbal monomers by evaluating their impact on cardiac signaling pathways subsequent to treatment. Graphical Abstract

Intranasal Delivery of Carvedilol- and Quercetin-Encapsulated Cationic Nanoliposomes for Cardiovascular Targeting: Formulation and In Vitro and Ex Vivo Studies

“…As antioxidants neutralize the damaging effects of ROS and maintain normal cellular physiological function, they are essential in preventing the development of many diseases, including cardiovascular diseases. QC is a flavonoid that is extensively distributed in plants and has the ability to lower the risk of cardiac issues connected to oxidative stress through a number of pathways, such as lowering LDL levels and oxidative stress, reducing endothelial dysfunction, suppressing inflammatory indicators, and preventing platelet aggregation . This study might provide insight for the antioxidant activity of individuals or a combination of CVD and QC intracellularly.…”

“…QC is a flavonoid that is extensively distributed in plants and has the ability to lower the risk of cardiac issues connected to oxidative stress through a number of pathways, such as lowering LDL levels and oxidative stress, reducing endothelial dysfunction, suppressing inflammatory indicators, and preventing platelet aggregation. 81 This study might provide insight for the antioxidant activity of individuals or a combination of CVD and QC intracellularly. Intracellular ROS generation in the H9c2 cardiomyoblast cells was evaluated using a fluorescent probe DCFH-DA determining the in vitro cardioprotective effect of CVD and QC alone or in combination at low and high doses against hydrogen peroxide.…”

Dose–response association between Chinese visceral adiposity index and cardiovascular disease: a national prospective cohort study

“…Visceral adiposity promotes systemic and vascular inflammation by increasing production of interleukin-6, tumor necrosis factor-α, and high-sensitivity C-reactive protein, which lead to atherogenesis and subsequently incident CVD ( 38 – 40 ). Besides, visceral adiposity disturbs the renin–angiotensinogen system and produces excessive reactive oxygen species and reactive nitrogen species, and then induce oxidative stress, which could be presented as oxidized low-density lipoprotein, 8-hydroxylated deoxyguanosine, malondialdehyde, thioredoxin, and advanced oxidation protein products; the oxidative stress would induce a vicious cycle of endothelial dysfunction, inflammation, fibroblast proliferation and affect cerebral arteries through stenosis and occlusion, leading to CVD incidence ( 38 , 41 – 44 ). Also, visceral obesity causes insulin resistance through increasing the production of inflammatory markers and adipocytokines and reducing that of adiponectin, which result in CVD incidence ( 45 – 47 ).…”

O-GlcNAcylation in ischemic diseases

“… (4) Oxidative stress contributes to the development of numerous diseases, including myocardial injury. Low reactive oxygen species (ROS) concentrations are involved in intracellular signaling and regulation, thereby aiding in the preservation of cellular homeostasis ( Yan et al, 2023 ), while reperfusion injury triggers an exponential surge in the generation of free radicals in isolated hearts ( Maslov et al, 2023 ). Ischemic injury elicits an inflammatory response via the stimulation of neutrophil activation, the release of cytokines, and the activation of the complement system.…”