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Data suggest that up-regulaton of Ang-(1 (show ANGPT1 Proteins)-7) levels in follicular fluid correlates with increases in number of mature oocytes retrieved upon ovarian stimulation in preparation for in vitro fertilization.
Urinary angiotensinogen (show AGT Proteins) and renin (show REN Proteins) excretion are elevated in CKD patients. Both parameters are negatively associated with eGFR (show EGFR Proteins) and these associations are independent of urinary albumin (show ALB Proteins) excretion
Reduced IL-18 (show IL18 Proteins) serum concentration in children after HUS (show CFH Proteins) with no difference in its urine concentration may indicate a loss of the protective effects of this cytokine on renal function due to previously occurred HUS (show CFH Proteins).
Angiotensin II initiates hepatocyte epithelial-mesenchymal transition by activating the NOX-derived H2O2-mediated NLRP3 (show NLRP3 Proteins) inflammasome/IL-1ss/Smad (show SMAD1 Proteins) circuit.
present study has demonstrated, for the first time, that high glucose augments AGT (show AGXT Proteins) in human RPTCs through HNF-5, which provides a potential therapeutic target for diabetic nephropathy
AngII-dependent phosphorylation of LCP1 (show LCP1 Proteins) in cultured podocytes was mediated by the kinases ERK (show EPHB2 Proteins), p90 (show CANX Proteins) ribosomal S6 kinase (show RPS6KB1 Proteins), PKA, or PKC (show PRRT2 Proteins). LCP1 (show LCP1 Proteins) phosphorylation increased filopodia formation.
Autosomal dominant polycystic kidney disease (ADPKD), uniquely increases urinary angiotensinogen (show AGT Proteins) and renin (show REN Proteins) excretion despite their circulating levels being comparable with those in non-ADPKD chronic kidney disease.
Quaternary interactions and supercoiling modulate the cooperative DNA binding of AGT (show AGXT Proteins).
results show that SNPs in the Hap (show SAFB Proteins)-I of the hAGT gene promote high-fat diet-induced binding of transcription factors GR, CEBP-beta (show CEBPB Proteins) and STAT3 (show STAT3 Proteins), which lead to elevated expression of the hAGT gene in hepatic and adipose tissues
Angiotensinogen (show AGT Proteins) import and subsequent trafficking to the mitochondria occurs in proximal kidney tubules.
NLRP3 (show NLRP3 Proteins) gene deletion attenuates Ang II (show AGT Proteins)-induced NLRP3 (show NLRP3 Proteins) inflammasome activation, phenotypic transformation from a contractile phenotype to a synthetic phenotype and proliferation in primary mice Vascular Smooth Muscle Cells.
adipocyte-derived Agt (show AGXT Proteins) has essentially no contribution to the plasma concentration and no impact on blood pressure compared to liver-derived Agt (show AGXT Proteins).
Lung ischemia-reperfusion injury causes a dysregulation of circulating Ang 2 (show ANGPT2 Proteins) levels and plasma PREP (show PREP Proteins) activity, although no direct link between both phenomena could be shown.
Inhibition of TLR4 (show TLR4 Proteins) ameliorates AngII-impaired cavernosal relaxation, decreases TNF-alpha (show TNF Proteins) levels, and restores Nitric Oxide bioavailability, demonstrating that TLR4 (show TLR4 Proteins) partly mediates AngII-induced cavernosal dysfunction.
Our study is the first to show the important role of IL-6 (show IL6 Proteins) in regulating cardiac pathogenesis via inflammation and apoptosis during AngII-induced hypertension. We also provide a novel link between IL-6 (show IL6 Proteins)/STAT3 (show STAT3 Proteins) and EndoG (show ENDOG Proteins)/MEF2A (show MEF2A Proteins) pathway that affects cardiac hypertrophy during AngII stimulation.
this study demonstrated that Ang II (show AGT Proteins) could increase TRPC6 (show TRPC6 Proteins) induced Ca(2 (show CA2 Proteins)+) influx and enhance autophagy through increasing reactive oxygen species levels in podocytes, and autophagy could protect Ang II (show AGT Proteins)-treated podocytes.
These results implied that AngII could effectively induce EpiCs to differentiate into vascular smooth muscle-like cells through the AT1 receptor (show AGTRAP Proteins).
Results suggest the involvement of angiotensin II (Ang II), through its angiotensin type-1 receptor (AT1R (show AGTRAP Proteins)) in the inflammation induced by Aah (show ASPH Proteins) 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 (show ACE Proteins) increased in streptozotocin-induced diabetic mice, which in turn led to an increase in Ang II (show AGT Proteins) levels and tactile allodynia.
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