To assess the association of the angiotensin II type 2 (AT2) receptor (-1332 G/A) gene polymorphism with premature coronary artery disease (CAD) and investigate for a further role in both myocardial infarction and predominantly stenotic atherosclerosis requiring revascularisation.
(2) In an accelerated atherosclerosis model, with angiotensin II-induced aortic lesions and aneurysms, A-002 (30 mg/kg twice a day) reduced aortic atherosclerosis by approximately 40% (P < 0.05) and attenuated aneurysm formation (P = 0.0096).
During active disease, patients with granulomatosis with polyangiitis (GPA; Wegener's granulomatosis) have accelerated atherosclerosis and ANGII inhibitors are recommended to these patients to reduce atherosclerosis.
Parenteral administration of enoxaparin (FXa/IIa inhibitor) and fondaparinux (FXa inhibitor) over 14 days reduced to severity of aortic aneurysm and atherosclerosis in AngII-infused ApoE<sup>-/-</sup> mice.
A missense gene mutation with methione-to-threonine amino acid substitution at codon 235 (M235T) of angiotensinogen (AGT) has been associated with higher plasma AGT levels and may influence the pathogenesis of cardiac hypertrophy and atherosclerosis.
Angiotensin II (Ang II), one of the main vasoactive hormones of the renin-angiotensin system, has been associated with the development and progression of atherosclerosis.
Previous studies have demonstrated that angiotensin II (Ang II) is involved in the process of atherosclerosis and vascular restenosis through its proinflammatory effect.
Angiotensin II (Ang II) stimulates vascular smooth muscle cell (VSMC) hypertrophy as a critical event in the development of vascular diseases such as atherosclerosis.
Additionally, lncRNAs have been associated with angiotensin II actions and with vascular diseases, including coronary heart disease and atherosclerosis. miRNAs, well studied in various vascular diseases, have also been recently shown to be differentially expressed in the biofluids of patients with vascular disease and mediate cell-cell communication.
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.
Angiotensin II and its type 1 receptor (AT1R) are both expressed in the adipose tissue and involved in the genesis of atherosclerosis as well as hypertension.
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.
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.
AQP1 is expressed in atherosclerotic lesion neovasculature in human and mouse arteries and AQP1 deficiency augments lesion development in ANGII-promoted atherosclerosis in mice.
To further elucidate the role of COUP-TFII, we performed DNA microarrays in VEC transfected with the siRNA of COUP-TFII and subsequently stimulated with angiotensin II (AngII) and compared the expression profiles of 112 genes involved in various atherosclerosis-related pathways.
Regulator of G-protein signaling 2 (RGS2) is a key molecule in signal pathways of vasoactive peptides, such as angiotensin II and endothelin 1, and is believed to have an important role in the pathophysiology of atherosclerosis.
A diet enriched with tree nuts reduces severity of atherosclerosis but not abdominal aneurysm in angiotensin II-infused apolipoprotein E deficient mice.