In particular, the infusion of angiotensin II (Ang II) in the apolipoprotein E-deficient mice (apoE-/-) and low density lipoprotein receptor knockout mice (LDLR-/-) to induce aortic aneurysm has been extensively used in the field.
Therefore, we investigated the effect of kinin B1 receptor deletion on the development of atherosclerosis and aortic aneurysms in apolipoprotein E-deficient (ApoE(-/-)) mice.
XBP1u, but not XBP1s, was markedly repressed in the aorta during the early onset of aortic aneurysm in both angiotensin II-infused apolipoprotein E knockout (ApoE<sup>-/-</sup>) and CaPO<sub>4</sub> (calcium phosphate)-induced C57BL/6J murine models, in parallel with a decrease in smooth muscle cell contractile apparatus proteins.
We examined the effect of FXa/FIIa inhibition on experimental aortic aneurysm in apolipoprotein E-deficient (ApoE<sup>-/-</sup>) mice infused with angiotensin II (AngII).
The current study aimed to investigate the therapeutic effects and potential mechanisms of murine bone marrow MSC (BM-MSCs)-derived conditioned medium (MSCs-CM) on angiotensin II (AngII)-induced AA in apolipoprotein E-deficient (apoE<sup>-/-</sup> ) mice.