This editorial refers to ‘Circulating microparticles generate and transport monomeric C-reactive protein in patients with myocardial infarction’ by J. Habersberger et al. , pp. 64–72, this issue. C-reactive protein, a member of the pentraxin superfamily, is a prototypical ‘acute-phase’ protein that is synthesized at a low rate under physiological conditions but is markedly induced and secreted following tissue injury and inflammation. Rapid secretion of C-reactive protein during the acute-phase response results in up to 1000-fold increases in plasma levels within 24–48 h. As a result, C-reactive protein is a highly sensitive, but non-specific, marker of systemic inflammation.1 Over the last 20 years, C-reactive protein has emerged as an important predictor of cardiovascular risk in a variety of clinical settings. The development of high-sensitivity C-reactive protein assays greatly enhanced the clinical value of plasma C-reactive protein.2 In contrast to traditional assays that were only suitable for measurements of acute-phase responses, high-sensitivity C-reactive protein immunoassays allowed quantification of baseline plasma levels of C-reactive protein with high sensitivity throughout its normal range. Elevated plasma high-sensitivity C-reactive protein levels predict cardiovascular risk and may identify patients who benefit the most from risk reduction therapies. Despite the abundance of evidence on the significance of C-reactive protein as a biomarker in cardiovascular disease, surprisingly little is known about its pathophysiological role. Although a causative role for C-reactive protein has been proposed in atherosclerosis and thrombosis,3 in vitro and in vivo studies have produced contradictory results. For example, treatment with human native C-reactive protein has been reported to accelerate atherosclerotic …