Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis

Marit Westerterp, Panagiotis Fotakis, Mireille Ouimet, Andrea E. Bochem, Hanrui Zhang, Matthew M. Molusky, Wei Wang, Sandra Abramowicz, Sacha la Bastide-van Gemert, Nan Wang, Carrie L. Welch, Muredach P. Reilly, Erik S. Stroes, Kathryn J. Moore, Alan R. Tall

Research output: Contribution to journalArticleAcademicpeer-review


BACKGROUND: The CANTOS trial (Canakinumab Antiinflammatory Thrombosis Outcome Study) showed that antagonism of interleukin (IL)-1β reduces coronary heart disease in patients with a previous myocardial infarction and evidence of systemic inflammation, indicating that pathways required for IL-1β secretion increase cardiovascular risk. IL-1β and IL-18 are produced via the NLRP3 inflammasome in myeloid cells in response to cholesterol accumulation, but mechanisms linking NLRP3 inflammasome activation to atherogenesis are unclear. The cholesterol transporters ATP binding cassette A1 and G1 (ABCA1/G1) mediate cholesterol efflux to high-density lipoprotein, and Abca1/g1 deficiency in myeloid cells leads to cholesterol accumulation.
Original languageEnglish
Pages (from-to)898-912
Issue number9
Publication statusPublished - 2018

Cite this