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The rs7079 C to A substitution reduced the binding of miR-31-5p/miR-584-5p to the 3' UTR of AGT, possibly altering the risk of lead poisoning.
These results suggest that Angiotensin II induces CTGF expression and extracellular matrix accumulation through a special TGF-beta-independent interaction between the NF-kappaB and Smad2/3 signals elicited by the AT1/PKCalpha/p38 MAPK pathway.
The possible contribution of the I/D in the ACE gene, M235T and T174M in the angiotensinogen (AGT) gene polymorphisms with ischemic stroke in young Mexican population.
AGT M235T gene polymorphism may represent a genetic modifier to vascular morbidities in Egyptian patients with sickle cell disease.
Patients with heart failure and type 2 diabetes mellitus with AGT TT + MT genotype had a higher level of ST2 and a higher probability of unfavorable cardiovascular events during 24 months of observation compared with MM genotype carriers.
Unfavorable genotype of polymorphic variants of candidate gene participating in endothelial dysfunction AGT (Thrl74Met and Met23SThr) was associated with changes in levels of their active substances in individuals exposed to mercury.
Angiotensin 1-7 can modulate cell adhesion and epithelial-mesenchymal transition of normal prostate epithelial cells.
These findings reveal the critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic tumor cells.
The reduced urinary AGT/creatinine in Autralian Indigenous pregnant women may reflect subclinical renal dysfunction which limits the ability of the kidney to maintain sodium balance and could indicate an increased risk of pregnancy complications and/or future renal disease.
ACE2 and other enzymes can form ANG-(1-7) directly or indirectly from either the decapeptide ANG I or from ANG II. [review]
The ACE and AGT gene polymorphisms are not associated with the progress of diabetes developing into retinopathy in Chinese patients with type 2 diabetes.
AGT M235T and T174M variants contribute to an increased risk of developing preeclampsia (PE), and for M235T to PE severity.
Data, including data using network analysis, suggest that angiotensinogen (AGT), mitogen-activated protein kinase-14 (MAPK14), and prothrombin (F2) in placental villous tissues are core factors in early embryonic development; these studies involved proteomics and bioinformatics analysis of altered protein expression in placental villous tissue from early recurrent miscarriage patients in comparison to control tissues.
The AGT (M235T) gene polymorphism do not seem to have a significant effect on the development of clinical properties or cardiovascular comordities of acromegalic patients.
Angiotensin II has a role in increasing glomerular permeability by beta-arrestin mediated nephrin endocytosis
After donor nephrectomy, increasing uAGT levels can be the result of activation of the intrarenal renin-angiotensin system affecting the compensatory changes in the remaining kidney.
M235T polymorphism of the AGT gene seems unrelated to the development or the clinical course of endometriosis.
AGT missense polymorphisms are not associated with diabetic nephropathy in our subset of Slovenian type 2 diabetes mellitus patients
Association of AGT single nucleotide polymorphism rs3789678 and gestational hypertension in Chinese population.
Data suggest that angiotensin-II plays important role in development of albuminuria, particularly in subjects with impaired glucose metabolism; here, serum angiotensin-II levels are up-regulated in subjects with prediabetes and type 2 diabetes as compared to subjects with normal glucose metabolism; elevated serum angiotensin-II level may be early biomarker or risk factor for vasculitis.
Our data demonstrate a previously unknown synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotection.
Mean blood pressure, plasma Ang II level, and myocardium malondialdehyde (MDA) content of angiotensinogen-renin (AGT-REN) double transgenic hypertension (dTH) mice were higher than those in wild-type (WT) mice.
ANG II is up-regulated in serum and heart tissues of mice with EAM and that ANG II significantly drives monocyte/macrophage infiltration through the C-C chemokine receptor 2/5 (CCR2/5) axis.
results established that A20 is involved in the renoprotective effect by calcitriol via negatively modulating the NF-kappaB pathway and necroptotic pathway in AngII-induced renal injury.
NLRP3 gene deletion attenuates Ang II-induced NLRP3 inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.
adipocyte-derived Agt has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt.
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 levels and plasma PREP activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6/STAT3 and EndoG/MEF2A pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II could increase TRPC6 induced Ca(2+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor.
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R) in the inflammation induced by Aah venom, in the heart and the aorta.
Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.
expression of spinal ACE increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II levels and tactile allodynia.
the beneficial actions of insulin in diabetic nephropathy appear to be mediated, in part, by suppressing renal Nrf2 and Agt gene transcription and preventing Nrf2 stimulation of Agt expression via hnRNP F/K.
Angiotensinogen-mediated downregulation of aquaporin 1 and Nrf2 signalling may play an important role in intrarenal renin-angiotensin system-induced hypertension and kidney injury.
This study suggests that deletion of AT2R decreases the expression of the beneficial ACE2/Ang-(1-7)/MasR.
an inverse correlation was found between Ang-(1-7) level and tau hyperphosphorylation, a pathological hallmark of Alzheimer's disease, in cerebral cortex and hippocampus of SAMP8 mice.
The inhibition of pathological autophagy in the heart in response to chronic Ang II by Interleukin-10, and its implications, has been described.
These results suggest that increased formation of AT1R-P2Y6R heterodimers with age may increase the likelihood of hypertension induced by Ang II.
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I, is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Mutations in this gene are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in this gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease.
alpha-1 antiproteinase, antitrypsin
, angiotensin I
, angiotensin II
, serine (or cysteine) proteinase inhibitor
, serpin A8
, angiotensinogen (PAT)
, angiotensin ll