A proatherogenic role for C-reactive protein in vivo.
OBJECTIVE
We have selectively reviewed some of the latest papers on the mechanistic role of C-reactive protein in atherosclerotic cardiovascular disease.


BACKGROUND
C-reactive protein is known to activate the classic pathway of the complement system. One paper examined the role of C-reactive protein in complement activation by enzymatically remodeled LDL proteins. Enzymatically remodeled LDL was found to induce complement activation with or without C-reactive protein, but in the presence of C-reactive protein the activation of complement halted before its terminal sequence. Complement activation by C-reactive protein in atherogenesis remains controversial. Different laboratories have reported the multi-organ origin of C-reactive protein. The atherosclerotic lesion itself is another place where C-reactive protein could be produced. Numerous studies have continued to dissect the potential diverse proatherogenic actions of C-reactive protein on cultured vascular cells. Caution must be exercised in inadequately controlled studies that have unwittingly used commercial C-reactive protein preparations contaminated by other bioactive components. In contrast to in-vitro experiments, in-vivo studies that support a proatherogenic role of C-reactive protein are less likely to be subject to misinterpretation.


CONCLUSIONS
Evidence suggests that C-reactive protein is a proatherogenic molecule that plays an active role. The amount of C-reactive protein in lesions is determined by its plasma levels and its local production. The biological effect of C-reactive protein on atherosclerosis development seems to encompass a complex network of interactions with other players in immunity and inflammation, such as the complement system, as well as a direct effect of C-reactive protein on the cells involved in lesion growth and development.
Paul
Antoni
A
Division of Diabetes, Endocrinology and Metabolism, Department of Medicine, Baylor College of Medicine, Houston, Texas 77030, USA.
Yeh
Edward T H
ET
Chan
Lawrence
L
D000818:Animals; D050197:Atherosclerosis / Q000209:etiology* / Q000276:immunology / Q000378:metabolism*; D002097:C-Reactive Protein / Q000009:adverse effects* / Q000502:physiology*; D003167:Complement Activation; D003165:Complement System Proteins / Q000009:adverse effects / Q000502:physiology*; D006801:Humans
D003165:Complement System Proteins; D002097:C-Reactive Protein