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Novel mechanisms of endothelial mechanotransduction
#MMPMID25301843
Abe J
; Berk BC
Arterioscler Thromb Vasc Biol
2014[Nov]; 34
(11
): 2378-86
PMID25301843
show ga
Atherosclerosis is a focal disease that develops preferentially where nonlaminar,
disturbed blood flow occurs, such as branches, bifurcations, and curvatures of
large arteries. Endothelial cells sense and respond differently to disturbed flow
compared with steady laminar flow. Disturbed flow that occurs in so-called
atheroprone areas activates proinflammatory and apoptotic signaling, and this
results in endothelial dysfunction and leads to subsequent development of
atherosclerosis. In contrast, steady laminar flow as atheroprotective flow
promotes expression of many anti-inflammatory genes, such as Kruppel-like factor
2 and endothelial nitric oxide synthase and inhibits endothelial inflammation and
athrogenesis. Here we will discuss that disturbed flow and steady laminar flow
induce pro- and antiatherogenic events via flow type-specific mechanotransduction
pathways. We will focus on 5 mechanosensitive pathways: mitogen-activated protein
kinases/extracellular signal-regulated kinase 5/Kruppel-like factor 2 signaling,
extracellular signal-regulated kinase/peroxisome proliferator-activated receptor
signaling, and mechanosignaling pathways involving SUMOylation, protein kinase
C-?, and p90 ribosomal S6 kinase. We think that clarifying regulation mechanisms
between these 2 flow types will provide new insights into therapeutic approaches
for the prevention and treatment of atherosclerosis.
|Animals
[MESH]
|Atherosclerosis/*physiopathology
[MESH]
|Biomechanical Phenomena/physiology
[MESH]
|Disease Models, Animal
[MESH]
|Endothelium, Vascular/*physiopathology
[MESH]
|Humans
[MESH]
|Mechanotransduction, Cellular/*physiology
[MESH]
|Mitogen-Activated Protein Kinase 7/physiology
[MESH]
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