TY - JOUR
T1 - Effect of HMG-CoA reductase inhibitors on vascular cell apoptosis
T2 - Beneficial or detrimental?
AU - Katsiki, Niki
AU - Tziomalos, Konstantinos
AU - Chatzizisis, Yiannis
AU - Elisaf, Moses
AU - Hatzitolios, Apostolos I.
PY - 2010/7
Y1 - 2010/7
N2 - Vascular cell apoptosis, an active form of programmed cell death, plays an integral role in atherosclerosis and in-stent restenosis after angioplasty, thus promoting the precipitation of acute cardiovascular events. Beyond their cholesterol-lowering effects, HMG-CoA reductase inhibitors, or statins, have been persistently reported to influence the apoptotic process.In this review we discuss the effect of statin treatment on vascular cell apoptosis, and therefore on atherosclerosis development, plaque rupture and in-stent restenosis, based on the results of up-to-date experimental and clinical studies. Lipophilic statins have been shown to induce apoptosis in a variety of cell types, including vascular smooth muscle cells and endothelial cells, whereas hydrophilic statins (rosuvastatin and pravastatin) have not. The clinical importance of statin induced apoptosis remains controversial, as it may blunt vascular wall thickening in the early stages of atherosclerosis or reduce the neointimal response to injury on the one hand, but on the other hand it may also promote destabilization of vulnerable plaques precipitating acute cardiovascular events.Current data support the initiation of statin treatment early enough to inhibit both the formation of atherosclerotic plaques (primary prevention) and in-stent restenosis (secondary prevention).
AB - Vascular cell apoptosis, an active form of programmed cell death, plays an integral role in atherosclerosis and in-stent restenosis after angioplasty, thus promoting the precipitation of acute cardiovascular events. Beyond their cholesterol-lowering effects, HMG-CoA reductase inhibitors, or statins, have been persistently reported to influence the apoptotic process.In this review we discuss the effect of statin treatment on vascular cell apoptosis, and therefore on atherosclerosis development, plaque rupture and in-stent restenosis, based on the results of up-to-date experimental and clinical studies. Lipophilic statins have been shown to induce apoptosis in a variety of cell types, including vascular smooth muscle cells and endothelial cells, whereas hydrophilic statins (rosuvastatin and pravastatin) have not. The clinical importance of statin induced apoptosis remains controversial, as it may blunt vascular wall thickening in the early stages of atherosclerosis or reduce the neointimal response to injury on the one hand, but on the other hand it may also promote destabilization of vulnerable plaques precipitating acute cardiovascular events.Current data support the initiation of statin treatment early enough to inhibit both the formation of atherosclerotic plaques (primary prevention) and in-stent restenosis (secondary prevention).
KW - Atherosclerosis
KW - Restenosis
KW - Statins
KW - Vascular cell apoptosis
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U2 - 10.1016/j.atherosclerosis.2009.12.028
DO - 10.1016/j.atherosclerosis.2009.12.028
M3 - Review article
C2 - 20060525
AN - SCOPUS:77954314235
SN - 0021-9150
VL - 211
SP - 9
EP - 14
JO - Atherosclerosis
JF - Atherosclerosis
IS - 1
ER -