This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Verma, S. Articles by Yeh, E. T.H. Search for Related Content PubMed PubMed Citation Articles by Verma, S. Articles by Yeh, E. T.H. Related Collections Pathophysiology Risk Factors Smooth muscle proliferation and differentiation Endothelium/vascular type/nitric oxide Other Vascular biology Related Article

(Circulation. 2004;109:1914-1917.)
© 2004 American Heart Association, Inc.

Focused Perspectives

C-Reactive Protein

Structure Affects Function

Subodh Verma, MD, PhD; Paul E. Szmitko, BSc; Edward T.H. Yeh, MD

From the Division of Cardiac Surgery, University of Toronto, Toronto, Canada (S.V., P.E.S.), and the Department of Cardiology, The University of Texas–M.D. Anderson Cancer Center, Houston, Tex (E.T.H.Y.).

Correspondence to Subodh Verma, MD, PhD, Division of Cardiac Surgery, Toronto General Hospital, 200 Elizabeth St, 14 EN-215, Toronto, Ontario, Canada M5G 2C4. E-mail subodh.verma@sympatico.ca

Key Words: Focused Perspectives • C-reactive protein • structure • inflammation • prognosis

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

	Introduction

 

"The pawn has been promoted to queen."¹

C-reactive protein (CRP), formerly considered solely as a biomarker for inflammation, is now viewed as a prominent partaker in endothelial dysfunction and atherosclerosis.^2,3 Serving clinically for several years as a nonspecific marker for inflammatory processes, CRP, with the advent of high-sensitivity assays, has emerged as one of the most powerful independent predictors of cardiovascular disease.^4,5 The Centers for Disease Control and Prevention and the American Heart Association issued a Class IIa recommendation for the screening of high-sensitivity (hs) CRP as a routine part of global cardiovascular risk assessment.⁶ However, several questions about CRP’s mechanism of action remain. In the present issue of Circulation, Khreiss et al⁷ provide evidence suggesting that native, pentameric CRP must undergo structural modification, forming monomeric subunits, before promoting a proinflammatory phenotype. This molecular finding may not only serve to influence basic molecular research examining CRP’s detrimental effect, but may also influence the clinical use of CRP as a prognostic marker.

See p 2016

	CRP as a Clinical Marker

 
Compelling evidence exists to support CRP’s designation as a powerful independent predictor of future cardiovascular risk. CRP predicts cardiovascular risk in a wide variety of clinical settings, including men and women without overt cardiovascular disease,^8,9 patients with stable angina or presenting with acute coronary syndromes,^10,11 postmyocardial infarction patients, and those with the metabolic syndrome.¹² Furthermore, CRP predicts not only incident myocardial infarction and cardiovascular death, but also the risk of ischemic stroke,¹³ sudden cardiac death,¹⁴ incident peripheral artery disease,¹⁵ and restenosis after percutaneous coronary intervention.¹⁶ . . . [Full Text of this Article]

Related Article:

Conformational Rearrangement in C-Reactive Protein Is Required for Proinflammatory Actions on Human Endothelial Cells

Tarek Khreiss, Levente József, Lawrence A. Potempa, and János G. Filep
Circulation 2004 109: 2016-2022. [Abstract] [Full Text]

This article has been cited by other articles:

				S. U. Eisenhardt, J. Habersberger, A. Murphy, Y.-C. Chen, K. J. Woollard, N. Bassler, H. Qian, C. von zur Muhlen, C. E. Hagemeyer, I. Ahrens, et al. Dissociation of Pentameric to Monomeric C-Reactive Protein on Activated Platelets Localizes Inflammation to Atherosclerotic Plaques Circ. Res., July 17, 2009; 105(2): 128 - 137. [Abstract] [Full Text] [PDF]

				J. F. Arenillas, J. Alvarez-Sabin, C. A. Molina, P. Chacon, I. Fernandez-Cadenas, M. Ribo, P. Delgado, M. Rubiera, A. Penalba, A. Rovira, et al. Progression of Symptomatic Intracranial Large Artery Atherosclerosis Is Associated With a Proinflammatory State and Impaired Fibrinolysis Stroke, May 1, 2008; 39(5): 1456 - 1463. [Abstract] [Full Text] [PDF]

				R. C. Becker Emerging Paradigms, Platforms, and Unifying Themes in Biomarker Science J. Am. Coll. Cardiol., October 30, 2007; 50(18): 1777 - 1780. [Full Text] [PDF]

				S.-R. Ji, Y. Wu, L. Zhu, L. A. Potempa, F.-L. Sheng, W. Lu, and J. Zhao Cell membranes and liposomes dissociate C-reactive protein (CRP) to form a new, biologically active structural intermediate: mCRPm FASEB J, January 1, 2007; 21(1): 284 - 294. [Abstract] [Full Text] [PDF]

				M. Rahmani, R. P. Cruz, D. J. Granville, and B. M. McManus Allograft Vasculopathy Versus Atherosclerosis Circ. Res., October 13, 2006; 99(8): 801 - 815. [Abstract] [Full Text] [PDF]

				T. A. Lakka, T. Rankinen, T. Rice, A. S. Leon, D. C. Rao, J. S. Skinner, and C. Bouchard Quantitative trait locus on chromosome 20q13 for plasma levels of C-reactive protein in healthy whites: the HERITAGE Family Study Physiol Genomics, October 11, 2006; 27(2): 103 - 107. [Abstract] [Full Text] [PDF]

				C. D. Bushnell, P. Hurn, C. Colton, V. M. Miller, G. del Zoppo, M. S.V. Elkind, B. Stern, D. Herrington, G. Ford-Lynch, P. Gorelick, et al. Advancing the Study of Stroke in Women: Summary and Recommendations for Future Research From an NINDS-Sponsored Multidisciplinary Working Group Stroke, September 1, 2006; 37(9): 2387 - 2399. [Abstract] [Full Text] [PDF]

				Y. Zhong, S.-H. Li, S.-M. Liu, P. E. Szmitko, X.-Q. He, P. W.M. Fedak, and S. Verma C-Reactive Protein Upregulates Receptor for Advanced Glycation End Products Expression in Human Endothelial Cells Hypertension, September 1, 2006; 48(3): 504 - 511. [Abstract] [Full Text] [PDF]

				E. Paffen and M. P.M. deMaat C-reactive protein in atherosclerosis: A causal factor? Cardiovasc Res, July 1, 2006; 71(1): 30 - 39. [Abstract] [Full Text] [PDF]

				B. M. Scirica, D. A. Morrow, S. Verma, S. Devaraj, I. Jialal, B. M. Scirica, D. A. Morrow, S. Verma, S. Devaraj, and I. Jialal The Verdict Is Still Out Circulation, May 2, 2006; 113(17): 2128 - 2151. [Full Text] [PDF]

				T. W. McDade, L. C. Hawkley, and J. T. Cacioppo Psychosocial and Behavioral Predictors of Inflammation in Middle-Aged and Older Adults: The Chicago Health, Aging, and Social Relations Study Psychosom Med, May 1, 2006; 68(3): 376 - 381. [Abstract] [Full Text] [PDF]

				S.-R. Ji, Y. Wu, L. A. Potempa, Y.-H. Liang, and J. Zhao Effect of Modified C-Reactive Protein on Complement Activation: A Possible Complement Regulatory Role of Modified or Monomeric C-Reactive Protein in Atherosclerotic Lesions Arterioscler Thromb Vasc Biol, April 1, 2006; 26(4): 935 - 941. [Abstract] [Full Text] [PDF]

				E. Shagdarsuren, M. Wellner, J.-H. Braesen, J.-K. Park, A. Fiebeler, N. Henke, R. Dechend, P. Gratze, F. C. Luft, and D. N. Muller Complement Activation in Angiotensin II-Induced Organ Damage Circ. Res., September 30, 2005; 97(7): 716 - 724. [Abstract] [Full Text] [PDF]

				S. B. Schwedler, K. Amann, K. Wernicke, A. Krebs, M. Nauck, C. Wanner, L. A. Potempa, and J. Galle Native C-Reactive Protein Increases Whereas Modified C-Reactive Protein Reduces Atherosclerosis in Apolipoprotein E-Knockout Mice Circulation, August 16, 2005; 112(7): 1016 - 1023. [Abstract] [Full Text] [PDF]

				I. Ikonomidis, J. Lekakis, I. Revela, F. Andreotti, and P. Nihoyannopoulos Increased circulating C-reactive protein and macrophage-colony stimulating factor are complementary predictors of long-term outcome in patients with chronic coronary artery disease Eur. Heart J., August 2, 2005; 26(16): 1618 - 1624. [Abstract] [Full Text] [PDF]

				S Vale Psychosocial stress and cardiovascular diseases Postgrad. Med. J., July 1, 2005; 81(957): 429 - 435. [Abstract] [Full Text] [PDF]