Transitional changes in the structure of C-reactive protein create highly pro-inflammatory molecules: Therapeutic implications for cardiovascular diseases

Transitional changes in the structure of C-reactive protein create highly pro-inflammatory molecules: Therapeutic implications for cardiovascular diseases

C-reactive protein (CRP) is the prototypic acute-phase reactant that has long been recognized almost exclusively as a marker of inflammation and predictor of cardiovascular risk. However, accumulating evidence indicates that CRP is also a direct pathogenic pro-inflammatory mediator in atherosclerosi...

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Bibliographic Details
Published in:Pharmacology & therapeutics (Oxford) Vol. 235; p. 108165
Main Authors: Zeller, J., Bogner, B., McFadyen, J.D., Kiefer, J., Braig, D., Pietersz, G., Krippner, G., Nero, T.L., Morton, C.J., Shing, K.S. Cheung Tung, Parker, M.W., Peter, K., Eisenhardt, S.U.
Format: Journal Article
Language:English
Published: England Elsevier Inc 01-07-2022
Subjects:
C-reactive protein
Cardiovascular disease
Inflammation
Innate immunity
ischemia/reperfusion injury
CRP
pCRP
C-reactive protein
IL
ischemia/reperfusion injury
Innate immunity
Cardiovascular disease
Inflammation
TNF
PC
ROS
ASO
mCR
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Summary:C-reactive protein (CRP) is the prototypic acute-phase reactant that has long been recognized almost exclusively as a marker of inflammation and predictor of cardiovascular risk. However, accumulating evidence indicates that CRP is also a direct pathogenic pro-inflammatory mediator in atherosclerosis and cardiovascular diseases. The ‘CRP system’ consists of at least two protein conformations with distinct pathophysiological functions. The binding of the native, pentameric CRP (pCRP) to activated cell membranes leads to a conformational change resulting in two highly pro-inflammatory isoforms, pCRP* and monomeric CRP (mCRP). The deposition of these pro-inflammatory isoforms has been shown to aggravate the localized tissue injury in a broad range of pathological conditions including atherosclerosis and thrombosis, myocardial infarction, and stroke. Here, we review recent findings on how these structural changes contribute to the inflammatory response and discuss the transitional changes in the structure of CRP as a novel therapeutic target in cardiovascular diseases and overshooting inflammation.
Bibliography:ObjectType-Article-2
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ISSN:0163-7258
1879-016X
DOI:10.1016/j.pharmthera.2022.108165