Angiotensin II deteriorates advanced atherosclerosis by promoting MerTK cleavage and impairing efferocytosis through the AT<sub>1</sub>R/ROS/p38 MAPK/ADAM17 pathway.
To accelerate the development of atherosclerosis, apolipoprotein E knockout mice were infused with angiotensin II (0.72 mg·kg<sup>-1</sup>·d<sup>-1</sup> subcutaneous) for 28 days.
Agonistic autoantibodies against angiotensin II type 1 (AT1) receptor (AT1-AAs) have been demonstrated to be pro-inflammatory and contribute to the progression of atherosclerosis.
The purpose of this study was to define the role of MasR deficiency in AngII-induced atherosclerosis and AAA formation and severity in hypercholesterolemic male mice.
The role of angiotensin II (Ang II) in hypertension has been clarified, but recent studies show that aging-associated arterial changes and those with hypertension as well as atherosclerosis may have some common pathogenesis.
To determine whether AGT and megalin interaction contributes to atherosclerosis, we used both male and female low-density lipoprotein receptor<sup>-/-</sup> mice fed a saturated fat-enriched diet and administered vehicles (PBS or control ASO) or megalin ASO.
Although the atheroprotective effects of statins and angiotensin II receptor blockers (ARBs) are well-established, little is known about their additive effects, especially during the early period of atherosclerosis.
Angiotensin II (Ang-II), a vascular stimulant associated with cardiovascular disease progression, has been demonstrated to be mainly involved in cardiovascular remodeling of atherosclerosis and cardiac hypertrophy.
In this study we explored the microRNAs responsible for the regulation of PAI-1 during LPS-stimulated inflammation in human aortic endothelial cells and subsequently studied the effect of a newly synthesized mitochondria-targeted esculetin (Mito-Esc) that was shown for its anti-atherosclerotic potential, in modulating PAI-1 levels and its targeted miRs during angiotensin-II-induced atherosclerosis in ApoE<sup>-/-</sup> mice.
This spontaneous model recapitulates aspects of human atherosclerosis, and allows for the development of dissecting abdominal aortic aneurysms (AAAs) when combined with angiotensin II.
Previous studies have demonstrated that angiotensin II (Ang II) is involved in the process of atherosclerosis and vascular restenosis through its proinflammatory effect.
Regarding pre-hospital medications, atherosclerosis-AHF patients were more likely to be administered nitroglycerin (20.3 vs. 13.7%, p = 0.003), nicorandil (18.8 vs. 7.5%, p < 0.001), angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II receptor blocker (ARB) (46.5 vs. 38.6%, p = 0.006), β-blocker (33.2 vs. 26.6%, p = 0.014) and statin (30.1 vs. 22.4%, p = 0.003) because of a previous coronary event or atherosclerotic diseases.
A diet enriched with tree nuts reduces severity of atherosclerosis but not abdominal aneurysm in angiotensin II-infused apolipoprotein E deficient mice.
This suggested that AngII infusion in this mouse model induced atherosclerosis development, and that plasma cholesterol levels represent a controlling factor.
These data suggested that AS-IV exerted beneficial effects on AngII -induced abnormal growth in rat VSMCs through disturbing cell cycle, especially block G1/S transition by attenuating CDK2 activity, which may hinder the process of pathological vascular remodeling during atherosclerosis.