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- W1768807077 abstract "Background: Heme oxygenase-1 (HO-1) has a role in vascular protection. Loss of HO-1 activity has previously been shown to accelerate the onset and severity of atherosclerotic plaques, while the opposite has been reported with elevated HO-1 activity. HO-1 confers cytoprotection to endothelial and smooth muscle cells, yet may also limit their proliferation. The role of HO-1 in late-stage atherosclerotic plaque stability has not yet been examined. Hypothesis: Loss of HO-1 cytoprotection confers plaque instability in late-stage atherosclerotic lesions of mice. Methods: Both HO-1 wild-type, ApoE deficient (HO-1+/+/ApoE-/-, knockout; KO) and HO-l deficient and ApoE deficient (HO-1-/-/ApoE-/-, double knockout; DKO) male mice were fed a Western diet for six months. Histology assessment of brachiocephalic arteries was performed to determine plaque composition. Results: Lesions from DKO-mice were smaller, more calcified, with greater extracellular matrix (ECM) compared to KO-mice whose lesions were larger, more lipid dense and acellular. Conclusions: HO-1 gene disruption in mice does not lead to atherosclerotic plaque with characteristics of instability. However, highly calcified plaques are directly correlated with poor prognosis. This may have implications for patients with low levels of HO-1, whose lesions may be clinically silent longer and in the event of rupture more deleterious." @default.
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- W1768807077 date "2014-04-01" @default.
- W1768807077 modified "2023-09-27" @default.
- W1768807077 title "Ectopic mineralization in late stage atherosclerosis of heme oxygenase‐1 deficient mice (832.11)" @default.
- W1768807077 doi "https://doi.org/10.1096/fasebj.28.1_supplement.832.11" @default.
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