Key result
COX-1 deficiency in bone marrow-derived cells significantly increased early atherosclerosis in apoE(-/-) and LDLR(-/-) mice compared with control mice transplanted with COX-1(+/+) marrow.
Population
Lethally irradiated LDL receptor (LDLR)(-/-) and apolipoprotein E (apoE)(-/-) recipient mice
Comparison
Transplantation with COX-1 bone marrow or fetal… vs Transplantation with COX-1 bone marrow or fetal…
Design
Preclinical
Authors
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Challenges presumed proatherogenic role of platelet COX-1; leaves open relevance of COX-1 inhibition to human atherosclerosis.
Effect estimate: 30% increase
COX-1 deficiency in bone marrow-derived cells worsens early atherosclerosis in mouse models, suggesting that platelet thromboxane production does not aggravate early lesion formation and that compensatory COX-2 upregulation in macrophages is proatherogenic.
Babaev et al. (2005) studied Atherosclerosis. COX-1(-/-) bone marrow transplantation vs. COX-1(+/+) bone marrow transplantation was evaluated on Extent of atherosclerotic lesions (30% increase). COX-1 deficiency in bone marrow-derived cells significantly increased early atherosclerosis in apoE(-/-) and LDLR(-/-) mice compared with control mice transplanted with COX-1(+/+) marrow.
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