NLRP3 inflammasome activation during myocardial ischemia reperfusion is cardioprotective.

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Abstract

The innate immune receptor NLRP3 recognizes tissue damage and initiates inflammatory processes through formation multiprotein complexes with the adaptor protein ASC and caspase-1, i.e. NLRP3 inflammasomes, which through cleavage of pro-IL-1β mediates release of bioactive IL-1β. We hypothesized that NLRP3 mediates tissue damage during acute myocardial infarction (MI) and sought to investigate the mechanisms herein in an experimental MI model in mice.

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Journal

Journal ID (iso-abbrev): Biochem. Biophys. Res. Commun.

Title: Biochemical and biophysical research communications

ISSN (Electronic): 1090-2104

ISSN (Print): 0006-291X

Publication date (Electronic): Jan 22 2016

Volume: 469

Issue: 4

Affiliations

[1 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Centre for Heart Failure Research, University of Oslo, Oslo, Norway; K.G.Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway. Electronic address: oystein.sandanger@rr-research.no.

[2 ] Temple University School of Medicine, Philadelphia, United States.

[3 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Centre for Heart Failure Research, University of Oslo, Oslo, Norway; K.G.Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway.

[4 ] Institute of Basic Medical Sciences, Department of Physiology, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.

[5 ] Centre for Heart Failure Research, University of Oslo, Oslo, Norway; Institute for Surgical Research, Oslo University Hospital Rikshospitalet, Oslo, Norway.

[6 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; K.G.Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway.

[7 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Centre for Heart Failure Research, University of Oslo, Oslo, Norway.

[8 ] Centre for Heart Failure Research, University of Oslo, Oslo, Norway.

[9 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; K.G.Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway; Section of Clinical Immunology and Infectious Diseases, Oslo University Hospital Rikshospitalet, Oslo, Norway.

[10 ] Research institute for internal medicine, Oslo University Hospital Rikshospitalet, Oslo, Norway; Centre for Heart Failure Research, University of Oslo, Oslo, Norway; K.G.Jebsen Inflammation Research Centre, University of Oslo, Oslo, Norway; Faculty of Medicine, University of Oslo, Oslo, Norway.

Article

Publisher Item ID: S0006-291X(15)31059-7

DOI: 10.1016/j.bbrc.2015.12.051

PubMed ID: 26706279

SO-VID: 703dd7dd-04c9-43e3-9b9e-51d5e08a95a5

History

Keywords: ASC,Acute coronary syndrome,Heart,Inflammasome,Inflammation,Ischemia-reperfusion,NLRP3,Revascularization

Data availability:

Keywords: ASC, Acute coronary syndrome, Heart, Inflammasome, Inflammation, Ischemia-reperfusion, NLRP3, Revascularization

NLRP3 inflammasome activation during myocardial ischemia reperfusion is cardioprotective.

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Abstract

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