The development of HIV protease inhibitor (PI)-related atherosclerosis may be a direct consequence of increased accumulation of cholesteryl ester in macrophages, rather than secondary to dyslipidemia. Researchers at the University of Kentucky Medical School report these findings in the January 15 online edition of the Journal of Clinical Investigation.
Dr. Eric J. Smart and colleagues found that treatment with ritonavir, indinavir or amprenavir increases the level of cholesteryl ester in THP-1 macrophages and peripheral blood mononuclear cells (PBMCs). However, when CD36 blocking antibodies were added or macrophages from CD36 knockout mice were used, the cells failed to accumulate sterol.
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