US EPA

191149 

Journal Article 

Review 

Atherosclerotic plaque stability—What determines the fate of a plaque? 

Halvorsen, B; Otterdal, K; Dahl, TB; Skjelland, M; Gullestad, L; Øie, E; Aukrust, P 

2008 

Yes 

Progress in Cardiovascular Diseases
ISSN: 0033-0620
EISSN: 1532-8643 

51 

3 

183-194 

English 

19026853 

10.1016/j.pcad.2008.09.001 

WOS:000261605500001 

Although the understanding of the underlying pathology of atherosclerosis has improved in recent years, the disease is still the main cause of death globally. Current evidence has implicated the role of inflammation in atherogenesis and plaque destabilization. Thus, inflammatory cytokines may attenuate interstitial collagen synthesis, increase matrix degradation, and promote apoptosis in several atheroma-associated cell types, and all these cellular events may enhance plaque vulnerability. Several cell types found within the lesion (ie, monocyte/macrophages, T cells, mast cells, platelets) contribute to this immune-mediated plaque destabilization, and a better understanding of these processes is a prerequisite for the development of new treatment strategies in these individuals. Such knowledge could also facilitate a better identification of high-risk individuals. In the present study, these issues will be discussed in more detail, particularly focusing on the interactions between matrix degradation, apoptotic, and inflammatory processes in plaque destabilization.