MiRrored Regulation of KLF2 and KLF4
Author(s) -
Anne Hamik,
Mukesh K. Jain
Publication year - 2012
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.112.245563
Subject(s) - klf2 , computer science , chemistry , gene , transcription factor , biochemistry
A healthy organism demands much from its endothelium; constance in homeostatic control of blood fluidity, vascular tone, interaction with circulating blood cells, maintenance of barrier functions, and, when appropriate, creation of new blood vessels. Breakdown in any of these functions, anywhere in the 60,000 miles of vessels in the human body, leads to or exacerbates a vast array of diseases including those plaguing modern man: atherosclerosis, diabetes, hypertension, cancer, and clotting disorders. In recent years, 2 endothelial transcription factors, Kruppel-like factor 2 (KLF2) and Kruppel-like factor 4 (KLF4), have garnered attention as guardians of endothelial health. Both Kruppel-like factors confer vascular protection via regulation of gene programs resulting in an antiinflammatory, anticoagulant, antiadhesive, antioxidant state of the endothelium.1–4 Thus, increased knowledge of the regulation of these regulators is of great interest. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Fang and Davies demonstrate that a single microRNA, miR92, regulates both KLF2 and KLF4—a finding that has exciting scientific and potentially therapeutic implications.See accompanying …
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