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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Veröffentlicht in:	Frontiers in immunology Jg. 13; S. 1039241
Hauptverfasser:	Zheng, Dongdong, Liu, Jia, Piao, Hulin, Zhu, Zhicheng, Wei, Ran, Liu, Kexiang
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Frontiers Media S.A 01.11.2022
Schlagworte:	endothelial cells ferroptosis Immunology parthanatos pyroptosis reactive oxygen species
ISSN:	1664-3224, 1664-3224
Online-Zugang:	Volltext
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Abstract	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.
AbstractList	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. 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.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.
Author	Zhu, Zhicheng Piao, Hulin Zheng, Dongdong Wei, Ran Liu, Jia Liu, Kexiang
AuthorAffiliation	2 Department of Cardiology, The Second Hospital of Jilin University , Changchun , China 1 Department of Cardiovascular Surgery of the Second Hospital of Jilin University, Changchun , Jilin , China
AuthorAffiliation_xml	– name: 1 Department of Cardiovascular Surgery of the Second Hospital of Jilin University, Changchun , Jilin , China – name: 2 Department of Cardiology, The Second Hospital of Jilin University , Changchun , China
Author_xml	– sequence: 1 givenname: Dongdong surname: Zheng fullname: Zheng, Dongdong – sequence: 2 givenname: Jia surname: Liu fullname: Liu, Jia – sequence: 3 givenname: Hulin surname: Piao fullname: Piao, Hulin – sequence: 4 givenname: Zhicheng surname: Zhu fullname: Zhu, Zhicheng – sequence: 5 givenname: Ran surname: Wei fullname: Wei, Ran – sequence: 6 givenname: Kexiang surname: Liu fullname: Liu, Kexiang
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Title	ROS-triggered endothelial cell death mechanisms: Focus on pyroptosis, parthanatos, and ferroptosis
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