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Large genome-wide association studies have identified that single-nucleotide polymorphisms proximal to Kr\u00fcppel-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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>KLF14 expression was markedly decreased in cholesterol loaded foam cells, and overexpression of KLF14 significantly increased cholesterol efflux and inhibited the inflammatory response in macrophages. We generated myeloid cell-selective Klf14 knockout (Klf14LysM) mice in the ApoE-\/- background for the atherosclerosis study. Klf14LysMApoE-\/- and litter-mate control mice (Klf14fl\/flApoE-\/-) were placed on the Western Diet for 12 weeks to induce atherosclerosis. Macrophage Klf14 deficiency resulted in increased atherosclerosis development without affecting the plasma lipid profiles. Klf14-deficient peritoneal macrophages showed significantly reduced cholesterol efflux resulting in increased lipid accumulation and exacerbated inflammatory response. Mechanistically, KLF14 upregulates the expression of a key cholesterol efflux transporter, ABCA1 (ATP-binding cassette transporter A1), while it suppresses the expression of several critical components of the inflammatory cascade. In macrophages, activation of KLF14 by its activator, perhexiline, a drug clinically used to treat angina, significantly inhibited the inflammatory response and increased cholesterol efflux in a KLF14-dependent manner in macrophages without triggering hepatic lipogenesis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study provides insights into the anti-atherosclerotic effects of myeloid KLF14 through promoting cholesterol efflux and suppressing the inflammatory response. Activation of KLF14 may represent a potential new therapeutic approach to prevent or treat atherosclerosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvab027","type":"journal-article","created":{"date-parts":[[2021,1,23]],"date-time":"2021-01-23T10:56:31Z","timestamp":1611399391000},"page":"475-488","source":"Crossref","is-referenced-by-count":27,"title":["Kr\u00fcppel-like factor 14 deletion in myeloid cells accelerates atherosclerotic lesion development"],"prefix":"10.1093","volume":"118","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0583-1386","authenticated-orcid":false,"given":"Huilun","family":"Wang","sequence":"first","affiliation":[{"name":"Molecular and Integrative Physiology, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yanhong","family":"Guo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5740-8010","authenticated-orcid":false,"given":"Haocheng","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8996-9253","authenticated-orcid":false,"given":"Yonghong","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]},{"name":"Second Xiangya Hospital, Central South University , Changsha, Hunan 410011,","place":["China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenting","family":"Hu","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9985-6674","authenticated-orcid":false,"given":"Wenying","family":"Liang","sequence":"additional","affiliation":[{"name":"Molecular and Integrative Physiology, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3381-3847","authenticated-orcid":false,"given":"Minerva T","family":"Garcia-Barrio","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lin","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8023-8080","authenticated-orcid":false,"given":"Anna","family":"Schwendeman","sequence":"additional","affiliation":[{"name":"Department of Pharmaceutical Sciences, University of Michigan , Ann Arbor, MI 48109,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5161-4705","authenticated-orcid":false,"given":"Jifeng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, Cardiovascular Center, University of Michigan Medical Center , Ann Arbor, MI 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