ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis

The endothelium is a single layer of epithelium covering the surface of the vascular system, and it represents a physical barrier between the blood and vessel wall that plays an important role in maintaining intravascular homeostasis. However, endothelial dysfunction or endothelial cell death can ca...

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Published in:Frontiers in immunology Vol. 13; p. 1039241
Main Authors: Zheng, Dongdong, Liu, Jia, Piao, Hulin, Zhu, Zhicheng, Wei, Ran, Liu, Kexiang
Format: Journal Article
Language:English
Published: Frontiers Media S.A 01.11.2022
Subjects:
endothelial cells
ferroptosis
Immunology
parthanatos
pyroptosis
reactive oxygen species
ISSN:1664-3224, 1664-3224
Online Access:Get full text
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Summary:The endothelium is a single layer of epithelium covering the surface of the vascular system, and it represents a physical barrier between the blood and vessel wall that plays an important role in maintaining intravascular homeostasis. However, endothelial dysfunction or endothelial cell death can cause vascular barrier disruption, vasoconstriction and diastolic dysfunction, vascular smooth muscle cell proliferation and migration, inflammatory responses, and thrombosis, which are closely associated with the progression of several diseases, such as atherosclerosis, hypertension, coronary atherosclerotic heart disease, ischemic stroke, acute lung injury, acute kidney injury, diabetic retinopathy, and Alzheimer’s disease. Oxidative stress caused by the overproduction of reactive oxygen species (ROS) is an important mechanism underlying endothelial cell death. Growing evidence suggests that ROS can trigger endothelial cell death in various ways, including pyroptosis, parthanatos, and ferroptosis. Therefore, this review will systematically illustrate the source of ROS in endothelial cells (ECs); reveal the molecular mechanism by which ROS trigger pyroptosis, parthanatos, and ferroptosis in ECs; and provide new ideas for the research and treatment of endothelial dysfunction-related diseases.
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Edited by: Benoit Pourcet, Université de Lille, France
Reviewed by: Aleksandr E. Vendrov, University of Michigan, United States; Roman A. Zinovkin, Lomonosov Moscow State University, Russia
These authors have contributed equally to this work
This article was submitted to Inflammation, a section of the journal Frontiers in Immunology
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2022.1039241