ArticleCellular signalling2014
Angiotensin-(1-7) abolishes AGE-induced cellular hypertrophy and myofibroblast transformation via inhibition of ERK1/2.
Article in Cellular signalling, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 53 citations in OpenAlex.
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- Interaction of estradiol and renin-angiotensin system with microRNAs-21 and -29 in renal fibrosis: focus on TGF-β/smad signaling pathway.Molecular biology reports · 2024Review
- Possible mechanisms of SARS-CoV-2-associated myocardial fibrosis: reflections in the post-pandemic era.Frontiers in microbiology · 2024Review
- A Review of Extracellular Vesicles in COVID-19 Diagnosis, Treatment, and Prevention.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Methylglyoxal-Modified Albumin Effects on Endothelial Arginase Enzyme and Vascular Function.Cells · 2023Article
- Article
- Emerging importance of ACE2 in external stratified epithelial tissues.Molecular and cellular endocrinology · 2021Review
- Evidence that angiotensin II does not directly stimulate the MD2-TLR4 innate inflammatory pathway.Peptides · 2021Article
- Molecular Mechanisms Involved in Intrarenal Renin-Angiotensin and Alternative Pathways in Diabetic Nephropathy - A Review.The review of diabetic studies : RDS · 2021Review
- Angiotensin-[1-7] attenuates kidney injury in experimental Alport syndrome.Scientific reports · 2020Article
- Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019Review
- Participation of GαFrontiers in pharmacology · 2019Article
- CR6-interacting factor 1 inhibits invasiveness by suppressing TGF-β-mediated epithelial-mesenchymal transition in hepatocellular carcinoma.Oncotarget · 2017Article
- MAS1 Receptor Trafficking Involves ERK1/2 Activation Through a β-Arrestin2-Dependent Pathway.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Significance of angiotensin 1-7 coupling with MAS1 receptor and other GPCRs to the renin-angiotensin system: IUPHAR Review 22.British journal of pharmacology · 2017Review
- Angiotensin-(1-7) and the Regulation of Anti-Fibrotic Signaling Pathways.Journal of cell signaling · 2017Article
- Chymase-dependent production of angiotensin II: an old enzyme in old hearts.American journal of physiology. Heart and circulatory physiology · 2017Article
- Connective tissue growth factor dependent collagen gene expression induced by MAS agonist AR234960 in human cardiac fibroblasts.PloS one · 2017Article
- Adverse cardiac effects of exogenous angiotensin 1-7 in rats with subtotal nephrectomy are prevented by ACE inhibition.PloS one · 2017Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledAngiotensin-(1-7) (Ang-(1-7))/AT7-Mas receptor axis is an alternative pathway within the renin-angiotensin system (RAS) that generally opposes the actions of Ang II/AT1 receptor pathway. Advanced glycated end product (AGEs) including glucose- and methylglyoxal-modified albumin (MGA) may contribute to the development and progression of diabetic nephropathy in part through activation of the Ang II/AT1 receptor system; however, the influence of AGE on the Ang-(1-7) arm of the RAS within the kidney is unclear. The present study assessed the impact of AGE on the Ang-(1-7) axis in NRK-52E renal epithelial cells. MGA exposure for 48 h significantly reduced the intracellular levels of Ang-(1-7) approximately 50%; however, Ang I or Ang II expression was not altered. The reduced cellular content of Ang-(1-7) was associated with increased metabolism of the peptide to the inactive metabolite Ang-(1-4) [MGA: 175±9 vs. CONTROL: 115±11 fmol/min/mg protein, p<0.05, n=3] but no change in the processing of Ang I to Ang-(1-7). Treatment with Ang-(1-7) reversed MGA-induced cellular hypertrophy and myofibroblast transition evidenced by reduced immunostaining and protein expression of α-smooth muscle actin (α-SMA) [0.4±0.1 vs. 1.0±0.1, respectively, n=3, p<0.05]. Ang-(1-7) abolished AGE-induced activation of the MAP kinase ERK1/2 to a similar extent as the TGF-β receptor kinase inhibitor SB58059; however, Ang-(1-7) did not attenuate the MGA-stimulated release of TGF-β. The AT7-Mas receptor antagonist D-Ala(7)-Ang-(1-7) abolished the inhibitory actions of Ang-(1-7). In contrast, AT1 receptor antagonist losartan did not attenuate the MGA-induced effects. We conclude that Ang-(1-7) may provide an additional therapeutic approach to the conventional RAS blockade regimen to attenuate AGE-dependent renal injury.
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