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Front Physiol. 2017 Aug 23;8:600. doi: 10.3389/fphys.2017.00600. eCollection 2017.

Oxidative Stress-Mediated Atherosclerosis: Mechanisms and Therapies.

Author information

1
Guang'anmen Hospital, Chinese Academy of Chinese Medical SciencesBeijing, China.
2
Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital, Beijing University of Chinese MedicineBeijing, China.
3
Department of Cardiology, General Hospital of People's Liberation ArmyBeijing, China.
4
Masonic Medical Research LaboratoryUtica, NY, United States.

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.

KEYWORDS:

apoptosis; atherosclerosis; autophagy; epigenetics; inflammation; mitochondria; oxidative stress; therapies

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