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high glucose-induced podocytes damage by activating miR-370 signaling targeted to inhibit the expression of AGTRAP.
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verexpression of ATRAP induced adiponectin expression both in adipose tissue and primary adipocyte. Our data revealed that adipose ATRAP plays an important role in preventing metabolic disorders and adiponectin possibly mediates the effects of adipose ATRAP.
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ATRAP plays an important role in inhibiting kidney aging, possibly through sirtuin1-mediated mechanism independent of blocking AT1R signaling, and further protecting normal life span.
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Results presented in this study suggested that the enhancement in adipose ATRAP plays a protective role against the development of diet-induced visceral obesity and insulin resistance through improvement of adipose inflammation and function via the suppression of overactivation of adipose AT1R signaling.
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Renal ATRAP downregulation is involved in the onset and progression of blood pressure elevation caused by renal mass reduction, and implicates ATRAP as a therapeutic target for hypertension in chronic kidney disease.
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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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ATRAP expression in brown adipose tissue does not influence the pathogenesis of dietary obesity or metabolic disorders.
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Identify Atrap as a novel regulatory protein of the cardiac Ca(2+)-ATPase SERCA2a. Suggest that Atrap enhances the activity of SERCA2a and, consequently, facilitates ventricular relaxation.
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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.
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although erythropoiesis and blood pressure are negatively controlled through the AT1 receptor inhibition in vivo, the pathways involved are complex and distinct
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Distal tubule-dominant enhancement of ATRAP inhibits pathological renal sodium reabsorption and blood pressure elevation in response to high salt loading.
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AT1R knockout mice were less vulnerable to controlled cortical impact-induced injury.
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The inhibition of degradation of angiotensin II type 1 receptor-associated protein (ATRAP) and inactivation of AT1R-mediated p38 MAPK and STAT3 signaling pathways, are involved cardiac hypertrophy.
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Activation of aortic vascular ATRAP partially inhibits the Nox4/p22(phox)-ROS-p38MAPK/JNK pathway and pathological aortic hypertrophy provoked by Ang II-mediated hypertension.
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ATRAP, a directly interacting and functionally inhibiting molecule of AT1R, plays a protective role against the development of systemic insulin resistance via regulatory effects on adipose tissue function.
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AGTRAP expression is regulated by USF1 and USF2
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renal tubule-dominant ATRAP activation provokes no evident effects on blood pressure at baseline but exerts an inhibitory effect on the pathological elevation of blood pressure in response to angiotensin II stimulation
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These data imply an involvement of AT1R in fetal development and of AT2R in adult function.
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angiotensin-receptor-associated-protein and TRPV2 channel have roles in Angiotensin-2-mediated Ca2+ signaling in the retinal pigment epithelium
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These results suggest that the stimulation of mouse iPS cells with AT(1)R may enhance LIF-induced DNA synthesis, by augmenting the generation of superoxide and activating JAK/STAT3, and that AT(1)R stimulation may enhance Col IV-induced differentiation into mesodermal progenitor cells via p38 MAPK activation.