Pathogenesis of acute stroke and the role of inflammasomes

Fann, David Yang-Wei, Lee, Seung-Yoon, Manzanero, Silvia, Chunduri, Prasad, Sobey, Christopher G. and Arumugam, Thiruma V. (2013) Pathogenesis of acute stroke and the role of inflammasomes. Ageing Research Reviews, 12 4: 941-966. doi:10.1016/j.arr.2013.09.004

Author Fann, David Yang-Wei
Lee, Seung-Yoon
Manzanero, Silvia
Chunduri, Prasad
Sobey, Christopher G.
Arumugam, Thiruma V.
Title Pathogenesis of acute stroke and the role of inflammasomes
Journal name Ageing Research Reviews   Check publisher's open access policy
ISSN 1568-1637
Publication date 2013-01-01
Year available 2013
Sub-type Critical review of research, literature review, critical commentary
DOI 10.1016/j.arr.2013.09.004
Open Access Status
Volume 12
Issue 4
Start page 941
End page 966
Total pages 26
Place of publication Shannon, Co. Clare, Ireland
Publisher Elsevier
Language eng
Subject 1302 Curriculum and Pedagogy
1303 Specialist Studies in Education
1305 Biotechnology
1312 Molecular Biology
2808 Neurology
Abstract Inflammation is an innate immune response to infection or tissue damage that is designed to limit harm to the host, but contributes significantly to ischemic brain injury following stroke. The inflammatory response is initiated by the detection of acute damage via extracellular and intracellular pattern recognition receptors, which respond to conserved microbial structures, termed pathogen-associated molecular patterns or host-derived danger signals termed damage-associated molecular patterns. Multi-protein complexes known as inflammasomes (e.g. containing NLRP1, NLRP2, NLRP3, NLRP6, NLRP7, NLRP12, NLRC4, AIM2 and/or Pyrin), then process these signals to trigger an effector response. Briefly, signaling through NLRP1 and NLRP3 inflammasomes produces cleaved caspase-1, which cleaves both pro-IL-1β and pro-IL-18 into their biologically active mature pro-inflammatory cytokines that are released into the extracellular environment. This review will describe the molecular structure, cellular signaling pathways and current evidence for inflammasome activation following cerebral ischemia, and the potential for future treatments for stroke that may involve targeting inflammasome formation or its products in the ischemic brain.
Keyword Caspase-1
Ischemic stroke
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Critical review of research, literature review, critical commentary
Collections: Official 2014 Collection
School of Biomedical Sciences Publications
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Created: Fri, 29 Nov 2013, 23:44:10 EST by Anthony Yeates on behalf of School of Biomedical Sciences