Journal Article (Review Article)

DZNE-2020-04061

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Danger signaling in atherosclerosis.

Zimmer, S. ; Grebe, A. ; Latz, E. (Last author)DZNE*

2015
Assoc. New York, NY

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Please use a persistent id in citations: doi:10.1161/CIRCRESAHA.116.301135

Abstract: All aspects of the pathogenesis of atherosclerosis are critically influenced by the inflammatory response in vascular plaques. Research in the field of innate immunity from the past 2 decades has uncovered many novel mechanisms elucidating how immune cells sense microbes, tissue damage, and metabolic derangements. Here, we summarize which triggers of innate immunity appear during atherogenesis and by which pathways they can contribute to inflammation in atherosclerotic plaques. The increased understanding gained from studies assessing how immune activation is associated with the pathogenesis of atherosclerosis has provided many novel targets for potential therapeutic intervention. Excitingly, the concept that inflammation may be the core of cardiovascular disease is currently being clinically evaluated and will probably encourage further studies in this area.

Keyword(s): Animals (MeSH) ; Atherosclerosis: etiology (MeSH) ; Atherosclerosis: immunology (MeSH) ; Atherosclerosis: microbiology (MeSH) ; Humans (MeSH) ; Immunity, Innate: immunology (MeSH) ; Signal Transduction: immunology (MeSH)

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Contributing Institute(s):

1. Innate Immunity in Neurodegeneration (AG Latz)

Research Program(s):

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

Appears in the scientific report 2015

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Database coverage:
; Allianz-Lizenz ; BIOSIS Previews ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; IF >= 15 ; JCR ; NCBI Molecular Biology Database ; Nationallizenz ; SCOPUS ; Science Citation Index ; Science Citation Index Expanded ; Web of Science Core Collection

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