Hemizygous deficiency of krüppel-like factor 2 augments experimental atherosclerosis

G. Brandon Atkins, Yunmei Wang, Ganapati H. Mahabeleshwar, Hong Shi, Huiyun Gao, Daiji Kawanami, Viswanath Natesan, Zhiyong Lin, Daniel I. Simon, Mukesh K. Jain

Research output: Contribution to journalArticlepeer-review

147 Scopus citations


Krüppel-like factor (KLF)2 is a central regulator of endothelial and monocyte/macrophage gene expression and function in vitro. Although the composite effects of KLF2 in these 2 cell types predict that it likely inhibits vascular inflammation, the role of KLF2 in this process in vivo is uncharacterized. In this study, we provide evidence that hemizygous deficiency of KLF2 increased diet-induced atherosclerosis in apolipoprotein E-deficient mice. Our studies highlight an important role for KLF2 in primary macrophage foam cell formation via the potential regulation of the key lipid binding protein adipocyte protein 2/fatty acid-binding protein 4. These novel observations establish that KLF2 is an atheroprotective factor.

Original languageEnglish (US)
Pages (from-to)690-693
Number of pages4
JournalCirculation research
Issue number7
StatePublished - Sep 26 2008
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Hemizygous deficiency of krüppel-like factor 2 augments experimental atherosclerosis'. Together they form a unique fingerprint.

Cite this