Endothelial shear stress signal transduction and atherogenesis: From mechanisms to therapeutics

Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not randomly distributed. Instead, they are preferentially localized at the curvature and bifurcations along the arterial tree, where shear stres...

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Published inPharmacology & therapeutics (Oxford) Vol. 235; p. 108152
Main Authors He, Lei, Zhang, Cheng-Lin, Chen, Qinghua, Wang, Li, Huang, Yu
Format Journal Article
LanguageEnglish
Published England Elsevier Inc 01.07.2022
Subjects
Atherosclerosis
Atherosclerosis - metabolism
Endothelial cells
Endothelial Cells - metabolism
Endothelium, Vascular - metabolism
Epigenesis, Genetic
Humans
Inflammation
Mechano-transduction
Oxidative stress
Shear stress
Signal Transduction
Stress, Mechanical
Therapies
eNOS
JNK
HIF-1α
ICAM-1
Mechano-transduction
TAZ
NF-κB
PI3K
Cx
mTOR
EC
IL
TRPV
PKA
TFEB
PKC
MAPK
LSS
SIRT1
FN-EDA
HOX
NOX
ROS
Shear stress
AMPK
GPCR
TLR4
XBP-1
HUVECs
ERK
FoxO1
HDAC
Oxidative stress
NO
PECAM-1
lncRNA
YAP
S1P
CSE
LDL
Nrf2
Atherosclerosis
S1PR1
miRNA
NLRP3
TGF-β
ApoE
EndMT
FoxP1
MEF2
Inflammation
ox-LDL
Akt
KLF4
Endothelial cells
KLF2
OSS
Therapies
BMP4
TRX1
VCAM-1
TNF-α
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Abstract Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not randomly distributed. Instead, they are preferentially localized at the curvature and bifurcations along the arterial tree, where shear stress is low or disturbed. Numerous studies demonstrate that endothelial cell phenotypic change (e.g., inflammation, oxidative stress, endoplasmic reticulum stress, apoptosis, autophagy, endothelial-mesenchymal transition, endothelial permeability, epigenetic regulation, and endothelial metabolic adaptation) induced by oscillatory shear force play a fundamental role in the initiation and progression of atherosclerosis. Mechano-sensors, adaptor proteins, kinases, and transcriptional factors work closely at different layers to transduce the shear stress force from the plasma membrane to the nucleus in endothelial cells, thereby controlling the expression of genes that determine cell fate and phenotype. An in-depth understanding of these mechano-sensitive signaling cascades shall provide new translational strategies for therapeutic intervention of atherosclerotic vascular disease. This review updates the recent advances in endothelial mechano-transduction and its role in the pathogenesis of atherosclerosis, and highlights the perspective of new anti-atherosclerosis therapies through targeting these mechano-regulated signaling molecules.
AbstractList Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not randomly distributed. Instead, they are preferentially localized at the curvature and bifurcations along the arterial tree, where shear stress is low or disturbed. Numerous studies demonstrate that endothelial cell phenotypic change (e.g., inflammation, oxidative stress, endoplasmic reticulum stress, apoptosis, autophagy, endothelial-mesenchymal transition, endothelial permeability, epigenetic regulation, and endothelial metabolic adaptation) induced by oscillatory shear force play a fundamental role in the initiation and progression of atherosclerosis. Mechano-sensors, adaptor proteins, kinases, and transcriptional factors work closely at different layers to transduce the shear stress force from the plasma membrane to the nucleus in endothelial cells, thereby controlling the expression of genes that determine cell fate and phenotype. An in-depth understanding of these mechano-sensitive signaling cascades shall provide new translational strategies for therapeutic intervention of atherosclerotic vascular disease. This review updates the recent advances in endothelial mechano-transduction and its role in the pathogenesis of atherosclerosis, and highlights the perspective of new anti-atherosclerosis therapies through targeting these mechano-regulated signaling molecules.
Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not randomly distributed. Instead, they are preferentially localized at the curvature and bifurcations along the arterial tree, where shear stress is low or disturbed. Numerous studies demonstrate that endothelial cell phenotypic change (e.g., inflammation, oxidative stress, endoplasmic reticulum stress, apoptosis, autophagy, endothelial-mesenchymal transition, endothelial permeability, epigenetic regulation, and endothelial metabolic adaptation) induced by oscillatory shear force play a fundamental role in the initiation and progression of atherosclerosis. Mechano-sensors, adaptor proteins, kinases, and transcriptional factors work closely at different layers to transduce the shear stress force from the plasma membrane to the nucleus in endothelial cells, thereby controlling the expression of genes that determine cell fate and phenotype. An in-depth understanding of these mechano-sensitive signaling cascades shall provide new translational strategies for therapeutic intervention of atherosclerotic vascular disease. This review updates the recent advances in endothelial mechano-transduction and its role in the pathogenesis of atherosclerosis, and highlights the perspective of new anti-atherosclerosis therapies through targeting these mechano-regulated signaling molecules.Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not randomly distributed. Instead, they are preferentially localized at the curvature and bifurcations along the arterial tree, where shear stress is low or disturbed. Numerous studies demonstrate that endothelial cell phenotypic change (e.g., inflammation, oxidative stress, endoplasmic reticulum stress, apoptosis, autophagy, endothelial-mesenchymal transition, endothelial permeability, epigenetic regulation, and endothelial metabolic adaptation) induced by oscillatory shear force play a fundamental role in the initiation and progression of atherosclerosis. Mechano-sensors, adaptor proteins, kinases, and transcriptional factors work closely at different layers to transduce the shear stress force from the plasma membrane to the nucleus in endothelial cells, thereby controlling the expression of genes that determine cell fate and phenotype. An in-depth understanding of these mechano-sensitive signaling cascades shall provide new translational strategies for therapeutic intervention of atherosclerotic vascular disease. This review updates the recent advances in endothelial mechano-transduction and its role in the pathogenesis of atherosclerosis, and highlights the perspective of new anti-atherosclerosis therapies through targeting these mechano-regulated signaling molecules.
ArticleNumber 108152
Author He, Lei
Chen, Qinghua
Wang, Li
Zhang, Cheng-Lin
Huang, Yu
Author_xml – sequence: 1
  givenname: Lei
  surname: He
  fullname: He, Lei
  organization: School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
– sequence: 2
  givenname: Cheng-Lin
  surname: Zhang
  fullname: Zhang, Cheng-Lin
  organization: Department of Pathophysiology, School of Basic Medical Sciences, Shenzhen University Health Science Center, Shenzhen 518060, China
– sequence: 3
  givenname: Qinghua
  surname: Chen
  fullname: Chen, Qinghua
  organization: Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China
– sequence: 4
  givenname: Li
  surname: Wang
  fullname: Wang, Li
  organization: Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China
– sequence: 5
  givenname: Yu
  surname: Huang
  fullname: Huang, Yu
  email: yu.huang@cityu.edu.hk
  organization: Department of Biomedical Sciences, City University of Hong Kong, Hong Kong, China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35122834$$D View this record in MEDLINE/PubMed
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JNK
HIF-1α
ICAM-1
Mechano-transduction
TAZ
NF-κB
PI3K
Cx
mTOR
EC
IL
TRPV
PKA
TFEB
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CSE
LDL
Nrf2
Atherosclerosis
S1PR1
miRNA
NLRP3
TGF-β
ApoE
EndMT
FoxP1
MEF2
Inflammation
ox-LDL
Akt
KLF4
Endothelial cells
KLF2
OSS
Therapies
BMP4
TRX1
VCAM-1
TNF-α
Language English
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Snippet Atherosclerotic vascular disease and its complications are among the top causes of mortality worldwide. In the vascular lumen, atherosclerotic plaques are not...
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SubjectTerms Atherosclerosis
Atherosclerosis - metabolism
Endothelial cells
Endothelial Cells - metabolism
Endothelium, Vascular - metabolism
Epigenesis, Genetic
Humans
Inflammation
Mechano-transduction
Oxidative stress
Shear stress
Signal Transduction
Stress, Mechanical
Therapies
Title Endothelial shear stress signal transduction and atherogenesis: From mechanisms to therapeutics
URI https://dx.doi.org/10.1016/j.pharmthera.2022.108152
https://www.ncbi.nlm.nih.gov/pubmed/35122834
https://www.proquest.com/docview/2626008293
Volume 235
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