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

doi:https://doi.org/10.1161/CIRCULATIONAHA.117.032636

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 journal › Article › Academic › peer-review

212 Citations (Scopus)

Abstract

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 language	English
Pages (from-to)	898-912
Journal	Circulation
Volume	138
Issue number	9
DOIs	https://doi.org/10.1161/CIRCULATIONAHA.117.032636
Publication status	Published - 2018

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Westerterp, M., Fotakis, P., Ouimet, M., Bochem, A. E., Zhang, H., Molusky, M. M., Wang, W., Abramowicz, S., la Bastide-van Gemert, S., Wang, N., Welch, C. L., Reilly, M. P., Stroes, E. S., Moore, K. J., & Tall, A. R. (2018). Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis. Circulation, 138(9), 898-912. https://doi.org/10.1161/CIRCULATIONAHA.117.032636

@article{d016d1d5aa924d7e80bba1090fbaa5ed,

title = "Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis",

abstract = "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.",

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

year = "2018",

doi = "https://doi.org/10.1161/CIRCULATIONAHA.117.032636",

language = "English",

volume = "138",

pages = "898--912",

journal = "Circulation",

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Westerterp, M, Fotakis, P, Ouimet, M, Bochem, AE, Zhang, H, Molusky, MM, Wang, W, Abramowicz, S, la Bastide-van Gemert, S, Wang, N, Welch, CL, Reilly, MP, Stroes, ES, Moore, KJ & Tall, AR 2018, 'Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis', Circulation, vol. 138, no. 9, pp. 898-912. https://doi.org/10.1161/CIRCULATIONAHA.117.032636

TY - JOUR

T1 - Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis

AU - Westerterp, Marit

AU - Fotakis, Panagiotis

AU - Ouimet, Mireille

AU - Bochem, Andrea E.

AU - Zhang, Hanrui

AU - Molusky, Matthew M.

AU - Wang, Wei

AU - Abramowicz, Sandra

AU - la Bastide-van Gemert, Sacha

AU - Wang, Nan

AU - Welch, Carrie L.

AU - Reilly, Muredach P.

AU - Stroes, Erik S.

AU - Moore, Kathryn J.

AU - Tall, Alan R.

PY - 2018

Y1 - 2018

N2 - 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.

AB - 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.

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UR - https://www.ncbi.nlm.nih.gov/pubmed/29588315

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DO - https://doi.org/10.1161/CIRCULATIONAHA.117.032636

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SN - 0009-7322

VL - 138

SP - 898

EP - 912

JO - Circulation

JF - Circulation

IS - 9

ER -

Cholesterol Efflux Pathways Suppress Inflammasome Activation, NETosis, and Atherogenesis

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