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Our data demonstrate a previously unknown synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotection.
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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.
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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.
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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.
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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.
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adipocyte-derived Agt has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt.
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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.
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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.
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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.
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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.
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These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor.
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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.
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Angiotensin II stimulates PYY secretion, in turn inhibiting epithelial anion fluxes, thereby reducing net fluid secretion into the colonic lumen.
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expression of spinal ACE increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II levels and tactile allodynia.
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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.
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Angiotensinogen-mediated downregulation of aquaporin 1 and Nrf2 signalling may play an important role in intrarenal renin-angiotensin system-induced hypertension and kidney injury.
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This study suggests that deletion of AT2R decreases the expression of the beneficial ACE2/Ang-(1-7)/MasR.
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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.
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The inhibition of pathological autophagy in the heart in response to chronic Ang II by Interleukin-10, and its implications, has been described.
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These results suggest that increased formation of AT1R-P2Y6R heterodimers with age may increase the likelihood of hypertension induced by Ang II.
