Kruppel-like factor 14 deletion in myeloid cells accelerates atherosclerotic lesion development.

ABSTRACT:

Aims

Atherosclerosis is the dominant pathologic basis of many cardiovascular diseases. Large genome-wide association studies have identified that single-nucleotide polymorphisms proximal to Krüppel-like factor 14 (KLF14), a member of the zinc finger family of transcription factors, are associated with higher cardiovascular risks. Macrophage dysfunction contributes to atherosclerosis development and has been recognized as a potential therapeutic target for treating many cardiovascular diseases. Herein, we address the biologic function of KLF14 in macrophages and its role during the development of atherosclerosis.

Methods and results

KLF14 expression was markedly decreased in cholesterol loaded foam cells, and overexpression of KLF14 significantly increased cholesterol efflux

SUBMITTER: Wang H 

PROVIDER: S-EPMC8803076 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature