Abstract
The vascular endothelium, a thin layer of endothelial cells (ECs) that line the inner surface of blood vessels, is a critical interface between blood and all tissues. EC activation, dysfunction, and vascular inflammation occur when the endothelium is exposed to various insults such as proinflammatory cytokines, oxidative stress, hypertension, hyperglycemia, aging, and shear stress. These insults lead to the pathogenesis of a range of disease states, including atherosclerosis. Several signaling pathways, especially nuclear factor κB mediated signaling, play crucial roles in these pathophysiological processes. Recently, microRNAs (miRNAs) have emerged as important regulators of EC function by fine-tuning gene expression. In this review, we discuss how miRNAs regulate EC function and vascular inflammation in response to a variety of pathophysiologic stimuli. An understanding of the role of miRNAs in EC activation and dysfunction may provide novel targets and therapeutic opportunities for controlling atherosclerosis and other chronic inflammatory disease states.
Original language | English (US) |
---|---|
Article number | 372 |
Journal | Current atherosclerosis reports |
Volume | 15 |
Issue number | 12 |
DOIs | |
State | Published - Dec 1 2013 |
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Keywords
- Atherosclerosis
- Endothelial activation
- MiR-181b
- MicroRNA
- Nuclear factor κB
- Vascular inflammation
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Endothelial MicroRNAs and atherosclerosis. / Sun, Xinghui; Belkin, Nathan; Feinberg, Mark W.
In: Current atherosclerosis reports, Vol. 15, No. 12, 372, 01.12.2013.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Endothelial MicroRNAs and atherosclerosis
AU - Sun, Xinghui
AU - Belkin, Nathan
AU - Feinberg, Mark W.
PY - 2013/12/1
Y1 - 2013/12/1
N2 - The vascular endothelium, a thin layer of endothelial cells (ECs) that line the inner surface of blood vessels, is a critical interface between blood and all tissues. EC activation, dysfunction, and vascular inflammation occur when the endothelium is exposed to various insults such as proinflammatory cytokines, oxidative stress, hypertension, hyperglycemia, aging, and shear stress. These insults lead to the pathogenesis of a range of disease states, including atherosclerosis. Several signaling pathways, especially nuclear factor κB mediated signaling, play crucial roles in these pathophysiological processes. Recently, microRNAs (miRNAs) have emerged as important regulators of EC function by fine-tuning gene expression. In this review, we discuss how miRNAs regulate EC function and vascular inflammation in response to a variety of pathophysiologic stimuli. An understanding of the role of miRNAs in EC activation and dysfunction may provide novel targets and therapeutic opportunities for controlling atherosclerosis and other chronic inflammatory disease states.
AB - The vascular endothelium, a thin layer of endothelial cells (ECs) that line the inner surface of blood vessels, is a critical interface between blood and all tissues. EC activation, dysfunction, and vascular inflammation occur when the endothelium is exposed to various insults such as proinflammatory cytokines, oxidative stress, hypertension, hyperglycemia, aging, and shear stress. These insults lead to the pathogenesis of a range of disease states, including atherosclerosis. Several signaling pathways, especially nuclear factor κB mediated signaling, play crucial roles in these pathophysiological processes. Recently, microRNAs (miRNAs) have emerged as important regulators of EC function by fine-tuning gene expression. In this review, we discuss how miRNAs regulate EC function and vascular inflammation in response to a variety of pathophysiologic stimuli. An understanding of the role of miRNAs in EC activation and dysfunction may provide novel targets and therapeutic opportunities for controlling atherosclerosis and other chronic inflammatory disease states.
KW - Atherosclerosis
KW - Endothelial activation
KW - MiR-181b
KW - MicroRNA
KW - Nuclear factor κB
KW - Vascular inflammation
UR - http://www.scopus.com/inward/record.url?scp=84885981688&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84885981688&partnerID=8YFLogxK
U2 - 10.1007/s11883-013-0372-2
DO - 10.1007/s11883-013-0372-2
M3 - Article
C2 - 24158362
AN - SCOPUS:84885981688
VL - 15
JO - Current Atherosclerosis Reports
JF - Current Atherosclerosis Reports
SN - 1523-3804
IS - 12
M1 - 372
ER -