Abstract
Chronic inflammatory reactions which affect the arterial wall can be viewed as an underlying cause of atherosclerosis. C-reactive protein is an easily measurable marker which reflects the activity of inflammatory responses.
At the same time, CRP represents an active partaker of the inflammatory process. The role CRP plays in the pathogenesis of atherosclerosis is ambivalent: at the very beginning, it displays anti-inflammatory properties which contribute to the protection of the arterial wall from atherogenic lipoproteins.
Later on, genetic disposition of the host and the influence of many known risk factors convert CRP?s antiinflammatory activity into a net pro-inflammatory effect which boosts the development of atherosclerosis. Both the protective anti-inflammatory and the noxious pro-inflammatory activities of CRP reside in its capacity to activate the complement cascade.