Oxidative Stress in Cell Death and Cardiovascular Diseases

Abstract

ROS functions as a second messenger and modulates multiple signaling pathways under the physiological conditions. However, excessive intracellular ROS causes damage to the molecular components of the cell, which promotes the pathogenesis of various human diseases. Cardiovascular diseases are serious threats to human health with extremely high rates of morbidity and mortality. Dysregulation of cell death promotes the pathogenesis of cardiovascular diseases and is the clinical target during the disease treatment. Numerous studies show that ROS production is closely linked to the cell death process and promotes the occurrence and development of the cardiovascular diseases. In this review, we summarize the regulation of intracellular ROS, the roles of ROS played in the development of cardiovascular diseases, and the programmed cell death induced by intracellular ROS. We also focus on anti-ROS system and the potential application of anti-ROS strategy in the treatment of cardiovascular diseases.

Elevated homocysteine, as a biomarker of cardiac injury, in panic disorder patients due to oxidative stress

“…Due to the fact that serotonin metabolism disorder is one of the pathogens in panic, the results of the present study are confirmed. In other words, increased serotonin levels elevate its catabolism and as a result the activity of the enzyme monoamine oxidase, which in turn leads to the induction and increase of oxidative stress (Hamzekolaei et al, 2020; Sturza, et al, 2019; Sturza, et al, 2019; Xu et al, 2019), demonstrated in our results by reduced level of glutathione and glutathione peroxidase activists and elevated levels of carbonyl proteins. Our previous study also reported an increase in malondialdehyde levels as an indicator of oxidative stress (Hamzekolaei et al, 2020).…”

Pleiotropic Properties of Valsartan: Do They Result from the Antiglycooxidant Activity? Literature Review and In Vitro Study

“…Oxidative stress, which is defined as excessive production of reactive oxygen species (ROS) and disproportion of oxidants over antioxidants, causes myocardial remodeling by activating hypertrophy-signaling kinases and stimulating cardiac fibroblasts to proliferate. ROS also affect myocardial calcium handling and lead to cellular dysfunction by inducing changes in intracellular pathways [59,60]. Moreover, in dysfunctional myocardium, enhanced ROS production is observed, and the antioxidant mechanism's exhaustion leads to disease progression [61,62].…”

Heat Shock Proteins in Oxidative Stress and Ischemia/Reperfusion Injury and Benefits from Physical Exercises: A Review to the Current Knowledge

“…This can lead to the formation of proteotoxic soluble peptides [ 70 ]. The cardioprotective effect of HSPs is manifested in an increased cell resistance to hypoxia [ 71 ] and oxidative stress [ 72 ] and in increase in functional recovery with a decreased infarction size after experimental induction of I/R [ 73 , 74 ]. The restoration of blood flow after ischemia leads to massive production of ROS, which generate severe damage to biomolecules—a phenomenon called myocardial reperfusion injury [ 10 ].…”