|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
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.
|
31595199 |
2019 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The beneficial effects of angiotensin II type 1 receptor blockers (ARBs) on atherosclerosis have been demonstrated in numerous studies.
|
31307370 |
2019 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings further support the use of exercise training and selective AT1 receptor blocker therapies for atherosclerotic cardiovascular disease prevention.
|
27246357 |
2017 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, formation of both AT1R homodimers and AT1R-GPCR heterodimer may be involved in the pathogenesis of human disease states, such as atherosclerosis and preeclampsia.
|
28648738 |
2017 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We hypothesized that the A1166C polymorphism could correlate with different, ultra-sonographically defined plaque phenotypes, as well as with an altered expression of AT1R mRNA and protein in human carotid plaques (CP), and altered expression of miR-155 in patients with advanced atherosclerosis.
|
27016615 |
2016 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Angiotensin II (AngII) type 1 receptor (AT1R) blockers have been proved to reduce atherosclerosis.
|
26771341 |
2016 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Angiotensin II is well-recognised to be a key mediator in driving the pathological events of diabetes-associated atherosclerosis via signalling through its angiotensin II type 1 receptor (AT1R) subtype.
|
27168137 |
2016 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The present review discusses the substrates of FXIIIa (activated FXIII) involved in thrombosis and wound healing with a particular focus on: (i) the influence of plasma FXIIIa on the formation of stable fibrin clots able to withstand mechanical and enzymatic breakdown through fibrin-fibrin cross-linking and cross-linking of fibrinolysis inhibitors, in particular α2-antiplasmin; (ii) the role of intracellular FXIIIa in clot retraction through cross-linking of platelet cytoskeleton proteins, including actin, myosin, filamin and vinculin; (iii) the role of intracellular FXIIIa in cross-linking the cytoplasmic tails of monocyte AT1Rs (angiotensin type 1 receptors) and potential effects on the development of atherosclerosis; and (iv) the role of FXIIIa on matrix deposition and tissue repair, including cross-linking of extracellular matrix proteins, such as fibronectin, collagen and von Willebrand factor, and the effects on matrix deposition and cell-matrix interactions.
|
23075332 |
2013 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The dynamic regulation of AT1R and AT2R expression suggests an active involvement of Ang II receptors in the development of cardiovascular diseases such as atherosclerosis, heart failure, chronic kidney diseases and cerebrovascular diseases.
|
23176214 |
2013 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Accumulating evidence indicates that angiotensin type 1 receptor (AT1R) blockers exert anti-inflammatory effects in inflammatory diseases including atherosclerosis.
|
20505677 |
2010 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
However, the influence of the AT1R gene A1166C polymorphism on atherosclerosis risk factors and on the development of early atherosclerosis is not clear.
|
19696781 |
2009 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Both ARB treatment and AT1aR deficiency suppressed diabetic atherosclerosis, ligand-RAGE expression and inflammatory changes.
|
17761193 |
2007 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To investigate whether the angiotensin-converting enzyme (ACE) insertion/deletion (I/D), angiotensinogen M235T or angiotensin II receptor type 1 573C/T polymorphism modify the risk of atherosclerosis associated with beta-blocker or ACE-inhibitor therapy.
|
17298481 |
2007 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
LHGDN |
Effect of a common X-linked angiotensin II type 2-receptor gene polymorphism (-1332 GA) on the occurrence of premature myocardial infarction and stenotic atherosclerosis requiring revascularization.
|
17336987 |
2007 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Angiotensin II type 1 receptor antagonists (AIIA) are beneficial for the prevention of atherosclerosis and diabetic nephropathy suggesting that angiotensin II (Ang II) promotes the development of these diseases.
|
17487826 |
2007 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
LHGDN |
Polymorphisms of the renin-angiotensin system are associated with blood pressure, atherosclerosis and cerebral white matter pathology.
|
17220293 |
2007 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Elevated levels of crosslinked AT1 receptor dimers on monocytes could sustain the process of atherogenesis, because inhibition of angiotensin II generation or of intracellular factor XIIIA activity suppressed the appearance of crosslinked AT1 receptors and symptoms of atherosclerosis in ApoE-deficient mice.
|
15507206 |
2004 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These results indicated that AT1 A/C1166 polymorphism was not associated with any clinical parameters associated with hypertension or atherosclerosis in the Japanese population.
|
12627873 |
2003 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In the present study, we compared the effects of eprosartan, an AT(1) receptor inhibitor, with the diuretic hydrochlorothiazide in a group of newly diagnosed hypertensive patients with multiple risk factors for atherosclerosis.
|
11897210 |
2002 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
To clarify how AT1 receptor antagonists reduce atherosclerosis, the effect of irbesartan on atherosclerotic lesion development was determined in low-fat, chow-fed apolipoprotein (Apo) E-deficient mice.
|
11486244 |
2001 |