Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis

Atherosclerosis (AS) is a chronic vascular disease characterized by lipid accumulation and the activation of the inflammatory response; it remains the leading nation-wide cause of death. Early in the progression of AS, stimulation by pro-inflammatory agonists (TNF-α, LPS, and others), oxidized lipop...

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Main Authors: Yan Shu, Si Jin
Format: Article
Language:English
Published: Elsevier 2023-08-01
Series:Heliyon
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2405844023058619
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author Yan Shu
Si Jin
author_facet Yan Shu
Si Jin
author_sort Yan Shu
collection DOAJ
description Atherosclerosis (AS) is a chronic vascular disease characterized by lipid accumulation and the activation of the inflammatory response; it remains the leading nation-wide cause of death. Early in the progression of AS, stimulation by pro-inflammatory agonists (TNF-α, LPS, and others), oxidized lipoproteins (ox-LDL), and biomechanical stimuli (low shear stress) lead to endothelial cell activation and dysfunction. Consequently, it is crucial to investigate how endothelial cells respond to different stressors and ways to alter endothelial cell activation in AS development, as they are the earliest cells to respond. Caveolin-1 (Cav1) is a 21-24-kDa membrane protein located in caveolae and highly expressed in endothelial cells, which plays a vital role in regulating lipid transport, inflammatory responses, and various cellular signaling pathways and has atherogenic effects. This review summarizes recent studies on the structure and physiological functions of Cav1 and outlines the potential mechanisms it mediates in AS development. Included are the roles of Cav1 in the regulation of endothelial cell autophagy, response to shear stress, modulation of the eNOS/NO axis, and transduction of inflammatory signaling pathways. This review provides a rationale for proposing Cav1 as a novel target for the prevention of AS, as well as new ideas for therapeutic strategies for early AS.
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spelling doaj.art-462550bb361a4fe98d84f679943c23f62023-08-30T05:52:06ZengElsevierHeliyon2405-84402023-08-0198e18653Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosisYan Shu0Si Jin1Department of Endocrinology, Institute of Geriatric Medicine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, 39 Lake Road, East Lake Ecological Scenic, Wuhan, 430077, ChinaCorresponding author. Department of Endocrinology, Institute of geriatric medicine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, 39 Lake Road, East Lake Ecological Scenic, Wuhan, 430077, Hubei Province, China.; Department of Endocrinology, Institute of Geriatric Medicine, Liyuan Hospital, Tongji Medical College, Huazhong University of Science and Technology, 39 Lake Road, East Lake Ecological Scenic, Wuhan, 430077, ChinaAtherosclerosis (AS) is a chronic vascular disease characterized by lipid accumulation and the activation of the inflammatory response; it remains the leading nation-wide cause of death. Early in the progression of AS, stimulation by pro-inflammatory agonists (TNF-α, LPS, and others), oxidized lipoproteins (ox-LDL), and biomechanical stimuli (low shear stress) lead to endothelial cell activation and dysfunction. Consequently, it is crucial to investigate how endothelial cells respond to different stressors and ways to alter endothelial cell activation in AS development, as they are the earliest cells to respond. Caveolin-1 (Cav1) is a 21-24-kDa membrane protein located in caveolae and highly expressed in endothelial cells, which plays a vital role in regulating lipid transport, inflammatory responses, and various cellular signaling pathways and has atherogenic effects. This review summarizes recent studies on the structure and physiological functions of Cav1 and outlines the potential mechanisms it mediates in AS development. Included are the roles of Cav1 in the regulation of endothelial cell autophagy, response to shear stress, modulation of the eNOS/NO axis, and transduction of inflammatory signaling pathways. This review provides a rationale for proposing Cav1 as a novel target for the prevention of AS, as well as new ideas for therapeutic strategies for early AS.http://www.sciencedirect.com/science/article/pii/S2405844023058619Caveolin-1AtherosclerosisAutophagyEndothelial cellseNOS/NO axisInflammation
spellingShingle Yan Shu
Si Jin
Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
Heliyon
Caveolin-1
Atherosclerosis
Autophagy
Endothelial cells
eNOS/NO axis
Inflammation
title Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
title_full Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
title_fullStr Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
title_full_unstemmed Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
title_short Caveolin-1 in endothelial cells: A potential therapeutic target for atherosclerosis
title_sort caveolin 1 in endothelial cells a potential therapeutic target for atherosclerosis
topic Caveolin-1
Atherosclerosis
Autophagy
Endothelial cells
eNOS/NO axis
Inflammation
url http://www.sciencedirect.com/science/article/pii/S2405844023058619
work_keys_str_mv AT yanshu caveolin1inendothelialcellsapotentialtherapeutictargetforatherosclerosis
AT sijin caveolin1inendothelialcellsapotentialtherapeutictargetforatherosclerosis