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Published on: April 3, 2017

m6A-Modified KLF11 Inhibits Macrophage Foam Cell Formation by Transcriptionally Suppressing ATP5B Expression in

Xiaohu Yang1, Zhuxin Gu1, Cong Chen1

  • 1Department of Interventional & Vascular Surgery, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|July 1, 2026
PubMed

Insights

Krüppel-like factor 11 (KLF11) inhibits macrophage foam cell formation and alleviates atherosclerosis. It achieves this by stabilizing KLF11 expression, which then suppresses inflammation and lipid accumulation, blocking NLRP3 inflammasome activation.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • Macrophage foam cell formation is a key feature of atherosclerosis (AS).
  • Krüppel-like factor 11 (KLF11) has shown protective effects against AS in diabetic conditions, but its role in macrophage foam cell formation was unclear.

Purpose of the Study:

  • To investigate the inhibitory effect of KLF11 on macrophage foam cell formation.
  • To elucidate the underlying molecular mechanisms of KLF11 in regulating AS.

Main Methods:

  • Established an in vivo AS model in ApoE-/- mice using a high-fat diet and a macrophage-specific KLF11 overexpression model via AAV.
  • Utilized RAW264.7 cells treated with oxidized low-density lipoprotein (ox-LDL) to induce foam cell formation.
  • Employed molecular assays including dual luciferase reporter gene assays, ChIP, RIP, HE staining, Masson staining, cholesterol efflux/uptake analysis, lipid/inflammation assessment, and Oil red O staining.

Main Results:

  • KLF11 expression was downregulated in AS; its overexpression suppressed inflammation, cholesterol, and lipid accumulation in AS mice.
  • Overexpression of KLF11 inhibited ox-LDL-induced foam cell formation in macrophages.
  • Mechanistically, IGF2BP3 stabilized KLF11 expression in an m6A-dependent manner, and KLF11 transcriptionally inhibited ATP5B, thereby preventing NLRP3 inflammasome activation.

Conclusions:

  • KLF11 plays a crucial role in inhibiting macrophage foam cell formation and alleviating AS.
  • IGF2BP3-mediated stabilization of KLF11 is a key mechanism.
  • KLF11 exerts its protective effects by transcriptionally inhibiting ATP5B and blocking NLRP3 inflammasome activation, offering a potential therapeutic target for AS.
Keywords:
ATP5BIGF2BP3KLF11atherosclerosisfoam cell formation

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