ArticleAmerican journal of physiology. Renal physiology2022
Angiotensin (1-7) protects against renal ischemia-reperfusion injury via regulating expression of NRF2 and microRNAs in Fisher 344 rats.
Article in American journal of physiology. Renal physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 18 citations in OpenAlex.
- Experimental rodent models of cardiorenal syndrome types 3 and 4: Insights and clinical relevance (Review).International journal of molecular medicine · 2026Review
- Mas-related G protein-coupled receptor type D deficiency promotes tubulointerstitial injury and fibrosis associated with proteinuria in male mice.Physiological reports · 2026Article
- Article
- Renal perfusion pressure: role and implications in critical illness.Annals of intensive care · 2025Review
- Observational
- Role of G-protein-coupled receptor kinase 4 on the dysfunction of renal Mas receptor in hypertension.PloS one · 2025Article
- Targeting the epidermal growth factor receptor (EGFR/ErbB) for the potential treatment of renal pathologies.Frontiers in pharmacology · 2024Review
- Counter-regulatory RAS peptides: new therapy targets for inflammation and fibrotic diseases?Frontiers in pharmacology · 2024Review
- Circulating extracellular vesicles in human cardiorenal syndrome promote renal injury in a kidney-on-chip system.JCI insight · 2023Article
- Liquid Biopsies Poorly miRror Renal Ischemia-Reperfusion Injury.Non-coding RNA · 2023Article
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Abstract
Ischemia-reperfusion (I/R) is considered the primary cause of acute kidney injury and is higher among older individuals. Although ischemic episodes are hard to predict and prevent, detrimental ischemic effects could be mitigated by exogenous intervention. This study aimed to identify the protective role of angiotensin (1-7) [ANG(1-7)] against I/R-induced renal injury in adult versus aged rats. Adult and aged male Fisher 344 rats were subjected to 40 min of bilateral renal ischemia followed by 28 days of reperfusion. ANG(1-7) was administered intraperitoneally in ischemic rats for 28 days with or without the Mas receptor antagonist A779. I/R increased blood pressure, plasma creatinine, urinary 8-isoprostane, and renal infiltration of pro- and anti-inflammatory macrophages and reduced glomerular filtration rate in both adult and aged rats compared with sham rats. In addition to causing glomerular sclerosis and tubular damage, I/R increased the expression of the following pathogenic miRNAs: miR-20a-5p, miR-21-5p, miR-24-3p, and miR-194-5p in both age groups. ANG(1-7) treatment of ischemic rats mitigated oxidative stress and renal inflammation, restored renal structure and function, and reduced high blood pressure. Also, ANG(1-7) suppressed the expression of pathogenic miRNAs. In addition, ANG(1-7) treatment of I/R rats increased the expression of the redox-sensitive transcription factor nuclear factor-erythroid factor 2-related factor 2 (NRF2) and phase II antioxidant enzymes. The beneficial effects of ANG(1-7) were sensitive to A779. Collectively, these data suggest that ANG(1-7) associated with NRF2 activation could alleviate post-I/R-induced kidney injury, and therefore serve as a potential therapeutic compound to protect against biochemical and morphological pathologies of I/R in both adults and aged populations.
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