title: High-density lipoproteins put out the fire.
abstract: Macrophages in atherosclerotic plaques are activated, inflammatory cells that directly contribute to the disease process. De Nardo et al. (2013), now report that high-density lipoproteins (HDL) can reprogram macrophages to be less inflammatory through an ATF3-dependent pathway, providing another mechanistic basis for the atheroprotective properties of HDL.
authors: Marc and Ruti Bell Vascular Biology and Disease Program, Leon H. Charney Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA.
authors: Kathryn J
authors: KJ
authors: Moore
authors: Marc and Ruti Bell Vascular Biology and Disease Program, Leon H. Charney Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, NY 10016, USA. Electronic address: edward.fisher@nyumc.org.
authors: Edward A
authors: EA
authors: Fisher
mesh_terms: D051700:Activating Transcription Factor 3 / Q000378:metabolism*; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D050197:Atherosclerosis / Q000628:therapy*; D002784:Cholesterol / Q000378:metabolism*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000628:therapy*; D008075:Lipoproteins, HDL / Q000627:therapeutic use*; D008264:Macrophages / Q000187:drug effects*
chemical_list: D051700:Activating Transcription Factor 3; D000894:Anti-Inflammatory Agents, Non-Steroidal; D008075:Lipoproteins, HDL; D002784:Cholesterol