Atherosclerotic plaque stability--what determines the fate of a plaque?
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.
Halvorsen
Bente
B
Research Institute for Internal Medicine, Department of Neurology, Rikshospitalet Medical Center, Oslo, Norway. bente.halvorsen@rr-research.no
Otterdal
Kari
K
Dahl
Tuva B
TB
Skjelland
Mona
M
Gullestad
Lars
L
Øie
Erik
E
Aukrust
Pål
P
D054058:Acute Coronary Syndrome / Q000473:pathology / Q000503:physiopathology; D017209:Apoptosis; D050197:Atherosclerosis / Q000201:enzymology / Q000473:pathology* / Q000503:physiopathology*; D001792:Blood Platelets / Q000276:immunology / Q000378:metabolism; D023921:Coronary Stenosis / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000473:pathology / Q000503:physiopathology; D008264:Macrophages / Q000378:metabolism*; D020782:Matrix Metalloproteinases / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism
D020782:Matrix Metalloproteinases