Abstract
Aim: Angiotensin (Ang) II plays a major role in atherogenesis and vulnerable plaque development. It remains unclear, however, whether Ang II induces plaque vulnerability directly through AT1 receptor (AT1R) on bone marrow (BM)-derived cells. This study therefore examined the effects of AT1R deficiency within BM-derived cells on Ang II-mediated vulnerable plaque in the 2-kidney, 1-clip [2K1C] ApoE-/- mouse model.
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