Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Atherosclerosis is a chronic, inflammatory disease of the arterial wall that underlies many of the common causes of cardiovascular morbidity and mortality, including myocardial infarction (MI), cerebrovascular and peripheral vascular disease. Early pathological descriptions viewed atherosclerosis as an end-stage degenerative process that inevitably resulted in a generalized narrowing of the arterial lumen. However, progress in our understanding of the pathophysiology and the underlying cellular and molecular mechanisms have revealed that atherosclerosis is a dynamic biological process. Key roles for the endothelium, inflammation and vascular smooth muscle cells (VSMC) in plaque biology have revealed that the cellular composition and biology of the plaque are more relevant to disease progression and complications than luminal narrowing alone, offering new opportunities to modify and treat different aspects of the disease process.

Original publication




Journal article


Medicine (United Kingdom)

Publication Date





397 - 402