Journal Article (Review Article)

DZNE-2020-03932

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Inflammasome activation in response to dead cells and their metabolites.

Kono, H. (Corresponding author) ; Kimura, Y. ; Latz, E. (Last author)DZNE*

2014
Elsevier New York, NY [u.a.]

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Please use a persistent id in citations: doi:10.1016/j.coi.2014.09.001

Abstract: Cell death cannot go unnoticed. It demands that the surrounding cells clear away the corpses in a manner appropriate to the type of cell death. Dying cells represent a threat to the body that should be eliminated by the host immune response. Inflammasome activation followed by IL-1alpha release and IL-1beta maturation is crucial for tackling pathological conditions, including infections, whereas inflammasome activation precedes inflammatory pyroptotic cell death. On the other hand, recent studies have shown that the inflammasome plays an important role in the pathogenesis of metabolic diseases, including obesity, diabetes, and atherosclerosis. Here, we review current knowledge of the association between cell death, excess metabolites, and inflammasome activation as it relates to chronic inflammatory diseases.

Keyword(s): Animals (MeSH) ; Atherosclerosis: immunology (MeSH) ; Cell Death (MeSH) ; Cholesterol, LDL: immunology (MeSH) ; Gout: immunology (MeSH) ; Humans (MeSH) ; Inflammasomes: immunology (MeSH) ; Tumor Lysis Syndrome: immunology (MeSH) ; Cholesterol, LDL ; Inflammasomes

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Contributing Institute(s):

1. Innate Immunity in Neurodegeneration (AG Latz ; AG Latz)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2014

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Database coverage:
; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF >= 5 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

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