Published in Cardiovascular Week, January 30th, 2006
"The death receptor Fas and Fas ligand (FasL) are present in human advanced atherosclerotic plaques. The activation of the Fas/FasL pathway of apoptosis has been implicated in plaque vulnerability. In the present study, we investigated whether overexpression of FasL in pre-existing atherosclerotic lesions can induce lesion remodeling and rupture-related events," researchers in the Netherlands report.
"Carotid atherogenesis was initiated in apolipoprotein E-deficient mice by placement of a perivascular silastic collar. The...
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Source: Cardiovascular Week (2006-01-30)
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