Title : Regression of atherosclerosis in apolipoprotein E-deficient mice is feasible using high-dose angiotensin receptor blocker, candesartan.

Pub. Date : 2012

PMID : 22576470






3 Functional Relationships(s)
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1 Treatment of cultured THP-1 macrophages in vitro with candesartan resulted in a similar decrease in ACAT1 expression. candesartan acetyl-Coenzyme A acetyltransferase 1 Mus musculus
2 In the kidney, glomerular lipid accumulation, mesangial expansion, and albuminuria were significantly regressed after treatment with high-dose candesartan, while biglycan and ACAT1 expressions were decreased. candesartan acetyl-Coenzyme A acetyltransferase 1 Mus musculus
3 CONCLUSION: These results suggest that regression of established atherosclerosis lesions in ApoE-deficient mice is feasible using high-dose candesartan, by mechanisms involving (i) a decrease in the lipid-retaining proteoglycan biglycan, and (ii) suppression of ACAT1 expression resulting in increased free cholesterol for lipid release. candesartan acetyl-Coenzyme A acetyltransferase 1 Mus musculus