ArticleJournal of cellular and molecular medicine2020
Dual deficiency of angiotensin-converting enzyme-2 and Mas receptor enhances angiotensin II-induced hypertension and hypertensive nephropathy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Ascertaining the mechanistic etiology of COVID-associated glomerulonephritis: a systematic review.Frontiers in medicine · 2025Pooled it
- STK40 inhibits profibrotic Arg1Acta pharmacologica Sinica · 2026Article
- Dapagliflozin ameliorates high glucose-induced epithelial-mesenchymal transition via up-regulating ACE2 mediated by EZH2 in diabetic nephropathy.Journal of endocrinological investigation · 2025Article
- Exploring hypertension-linked diseases: a comprehensive review of innovative drug combinations with enhanced therapeutic potential.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Non-lethal sonodynamic therapy mitigates hypertensive renal fibrosis through the PI3K/AKT/mTORC1-autophagy pathway.Scientific reports · 2025Article
- Application of Nanomaterial-Mediated Ferroptosis Regulation in Kidney Disease.International journal of nanomedicine · 2025Review
- Role of G-protein-coupled receptor kinase 4 on the dysfunction of renal Mas receptor in hypertension.PloS one · 2025Article
- Angiotensin-(1-7) and Central Control of Cardiometabolic Outcomes: Implications for Obesity Hypertension.International journal of molecular sciences · 2024Review
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- ACE2 alleviates sepsis-induced cardiomyopathy through inhibiting M1 macrophage via NF-κB/STAT1 signals.Cell biology and toxicology · 2024Article
- Correction to Dual deficiency of angiotensin-converting enzyme-2 and Mas receptor enhances angiotensin II-induced hypertension and hypertensive nephropathy.Journal of cellular and molecular medicine · 2023Article
- Mas receptor: a potential strategy in the management of ischemic cardiovascular diseases.Cell cycle (Georgetown, Tex.) · 2023Review
- Effect of botanical drugs in improving symptoms of hypertensive nephropathy: Analysis of real-world data, retrospective cohort, network, and experimental assessment.Frontiers in pharmacology · 2023Article
- Genetic Modifications to Alter Blood Pressure Level.Biomedicines · 2022Review
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- Molecular Mechanisms of Hypertensive Nephropathy: Renoprotective Effect of Losartan through Hsp70.Cells · 2021Review
- Angiotensin-(1-7)-A Potential Remedy for AKI: Insights Derived from the COVID-19 Pandemic.Journal of clinical medicine · 2021Review
- Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury.International journal of biological sciences · 2021Review
- Dual deficiency of angiotensin-converting enzyme-2 and Mas receptor enhances angiotensin II-induced hypertension and hypertensive nephropathy.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin-converting enzyme-2 (ACE2) and Mas receptor are the major components of the ACE2/Ang 1-7/Mas axis and have been shown to play a protective role in hypertension and hypertensive nephropathy individually. However, the effects of dual deficiency of ACE2 and Mas (ACE2/Mas) on Ang II-induced hypertensive nephropathy remain unexplored, which was investigated in this study in a mouse model of hypertension induced in either ACE2 knockout (KO) or Mas KO mice and in double ACE2/Mas KO mice by subcutaneously chronic infusion of Ang II. Compared with wild-type (WT) animals, mice lacking either ACE2 or Mas significantly increased blood pressure over 7-28 days following a chronic Ang II infusion (P < .001), which was further exacerbated in double ACE2/Mas KO mice (P < .001). Furthermore, compared to a single ACE2 or Mas KO mice, mice lacking ACE2/Mas developed more severe renal injury including higher levels of serum creatinine and a further reduction in creatinine clearance, and progressive renal inflammation and fibrosis. Mechanistically, worsen hypertensive nephropathy in double ACE2/Mas KO mice was associated with markedly enhanced AT1-ERK1/2-Smad3 and NF-κB signalling, thereby promoting renal fibrosis and renal inflammation in the hypertensive kidney. In conclusion, ACE2 and Mas play an additive protective role in Ang II-induced hypertension and hypertensive nephropathy. Thus, restoring the ACE2/Ang1-7/Mas axis may represent a novel therapy for hypertension and hypertensive nephropathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.