Mechanical Activation of Hypoxia-Inducible Factor 1α Drives Endothelial Dysfunction at Atheroprone Sites
Author(s) -
Shuang Feng,
Neil Bowden,
Maria Fragiadaki,
Céline Souilhol,
Sarah Hsiao,
Marwa Mahmoud,
Scott P. Allen,
Daniela Pirri,
Blanca Tardajos Ayllón,
Shamima Akhtar,
A. A. Roger Thompson,
Hanjoong Jo,
Christian Weber,
Victoria Ridger,
Andreas Schober,
Paul C. Evans
Publication year - 2017
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.117.309249
Subject(s) - hypoxia (environmental) , hypoxia inducible factors , endothelial dysfunction , medicine , cardiology , biology , endocrinology , chemistry , microbiology and biotechnology , biochemistry , gene , oxygen , organic chemistry
Atherosclerosis develops near branches and bends of arteries that are exposed to low shear stress (mechanical drag). These sites are characterized by excessive endothelial cell (EC) proliferation and inflammation that promote lesion initiation. The transcription factor HIF1α (hypoxia-inducible factor 1α) is canonically activated by hypoxia and has a role in plaque neovascularization. We studied the influence of shear stress on HIF1α activation and the contribution of this noncanonical pathway to lesion initiation.
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