Abstract
Atherogenesis, the formation of atherosclerotic plaques, is a complex process that involves several mechanisms, including endothelial dysfunction, neovascularization, vascular proliferation, apoptosis, matrix degradation, inflammation, and thrombosis. The pathogenesis and progression of atherosclerosis are explained differently by different scholars. One of the most common theories is the destruction of well-balanced homeostatic mechanisms, which incurs the oxidative stress. And oxidative stress is widely regarded as the redox status realized when an imbalance exists between antioxidant capability and activity species including reactive oxygen (ROS), nitrogen (RNS) and halogen species, non-radical as well as free radical species. This occurrence results in cell injury due to direct oxidation of cellular protein, lipid, and DNA or via cell death signaling pathways responsible for accelerating atherogenesis. This paper discusses inflammation, mitochondria, autophagy, apoptosis, and epigenetics as they induce oxidative stress in atherosclerosis, as well as various treatments for antioxidative stress that may prevent atherosclerosis.
Highlights
Atherosclerosis, the formation of atherosclerotic plaques, remains a major reason of the morbidity and mortality in both developed and developing nations (Townsend et al, 2015)
This study focuses on the method by which inflammation, mitochondria, autophagy, apoptosis, and epigenetics induce oxidative stress to accelerate atherosclerotic lesion formation
Cardiovascular and cerebrovascular diseases caused by atherosclerosis present a serious threat to human health worldwide
Summary
Atherosclerosis, the formation of atherosclerotic plaques, remains a major reason of the morbidity and mortality in both developed and developing nations (Townsend et al, 2015). This study focuses on the method by which inflammation, mitochondria, autophagy, apoptosis, and epigenetics induce oxidative stress to accelerate atherosclerotic lesion formation. Thiol oxidative stress results in macrophage functional disorder, cellular damage, as well as progressed development of atherosclerotic lesions (Wang et al, 2006).
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