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(Circulation Research. 2005;97:609.)
© 2005 American Heart Association, Inc.

Editorials

A New Perspective on the Biology of C-Reactive Protein

Edward T.H. Yeh

From the Department of Cardiology, The University of Texas M.D. Anderson Cancer Center, Research Center for Cardiovascular Diseases at The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center at Houston, and Texas Heart Institute, St Luke’s Episcopal Hospital, Houston, Texas.

Correspondence to Dr Edward T.H. Yeh, Department of Cardiology, Unit 449, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd, Houston, TX 77030. E-mail etyeh@mdanderson.org

See related article, pages 690–697

Key Words: C-reactive protein • vascular biology • modified CRP

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
C-reactive protein (CRP), composed of 5 23-kDa subunits, was traditionally viewed as one of the acute phase reactants.¹ More recently, CRP has risen in statue to subsume the role of the "best" marker of inflammation useful in the prediction of future cardiovascular risks.² However, the clinical utility of CRP measurement in cardiovascular risk prediction is still not well defined. Furthermore, there is an intense debate on whether CRP is merely a marker of inflammation or a direct participant.¹ The finding reported by Dr Janos Filep’s group in this issue of Circulation Research provides additional insights into the current CRP debate.³ In this editorial, I will focus my discussion on 2 main issues. Where is CRP produced? And, is CRP biologically active?

	Where Is CRP Produced?

 
CRP was traditionally thought to be produced by the liver in response to inflammatory cytokines. Several recent studies, however, clearly showed that CRP can be produced by nonhepatic tissues. Two studies have shown that both epithelial cells of the respiratory tract and renal epithelium can produce CRP under certain circumstances.^4,5 Moreover, neuronal cells also seem to be capable of synthesizing acute phase reactants involved in the pathogenesis of neurodegenerative disease such as Alzheimer disease.⁶ These new sources of CRP production pointed to a more systemic generation of CRP in our body. However, these new sources provided only tenuous link to atherosclerosis. CRP has been shown to colocalize with the terminal complement complex in atherosclerotic plaques.⁷ Furthermore, Yasojima et al reported that mRNAs for CRP and the classical complement components . . . [Full Text of this Article]

Related Article:

Loss of Pentameric Symmetry in C-Reactive Protein Induces Interleukin-8 Secretion Through Peroxynitrite Signaling in Human Neutrophils

Tarek Khreiss, Levente József, Lawrence A. Potempa, and János G. Filep
Circ. Res. 2005 97: 690-697. [Abstract] [Full Text] [PDF]

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