Myeloid Krüppel-like factor 4 deficiency augments atherogenesis in ApoE-/- mice--brief report.

Journal Article

OBJECTIVE: To investigate the role of Krüppel-like factor 4 (KLF4), an essential transcriptional regulator of macrophage polarization (M1/M2), in the pathogenesis of atherosclerosis. METHODS AND RESULTS: Despite the acknowledged importance of macrophages in atherosclerosis, the role of M1 (classically activated or proinflammatory) versus M2 (alternatively activated or anti-inflammatory) macrophages in this process remains incompletely understood. We recently identified KLF4 as a regulator of macrophage subset specification; that is, KLF4 promotes M2 and inhibits M1 phenotype. Here, we provide evidence that KLF4-deficient macrophages exhibit enhanced proinflammatory activation and foam cell formation in response to oxidized lipids. In vivo, myeloid KLF4-deficient mice (ApoE(-/-) background) develop significantly more vascular inflammation and atherosclerotic lesion formation. CONCLUSIONS: Our findings identify myeloid KLF4 as an essential regulator of vascular inflammation and experimental atherogenesis.

Full Text

Duke Authors

Cited Authors

  • Sharma, N; Lu, Y; Zhou, G; Liao, X; Kapil, P; Anand, P; Mahabeleshwar, GH; Stamler, JS; Jain, MK

Published Date

  • December 2012

Published In

Volume / Issue

  • 32 / 12

Start / End Page

  • 2836 - 2838

PubMed ID

  • 23065827

Pubmed Central ID

  • 23065827

Electronic International Standard Serial Number (EISSN)

  • 1524-4636

Digital Object Identifier (DOI)

  • 10.1161/ATVBAHA.112.300471


  • eng

Conference Location

  • United States