ArticlePhysiological reports2014
ACE2 deficiency increases NADPH-mediated oxidative stress in the kidney.
Article in Physiological reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 68 citations in OpenAlex.
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- Angiotensin-converting enzyme 2 regulates the placental response to repeated hypoxia-reoxygenation insult.The Journal of physiology · 2025Article
- Unlocking the protective potential of the angiotensin type 2 receptor (ATBiochemical pharmacology · 2024Article
- Parental recovered acute kidney injury causes prenatal renal dysfunction and fetal growth restriction with sexually dimorphic implications for adult offspring.Frontiers in physiology · 2024Article
- The RAAS Goodfellas in Cardiovascular System.Journal of clinical medicine · 2023Review
- Immune landscape and redox imbalance during neurological disorders in COVID-19.Cell death & disease · 2023Review
- The Impact of Angiotensin-Converting Enzyme-2/Angiotensin 1-7 Axis in Establishing Severe COVID-19 Consequences.Pharmaceutics · 2022Review
- Kidney Angiotensin in Cardiovascular Disease: Formation and Drug Targeting.Pharmacological reviews · 2022Review
- A diabetic milieu increases ACE2 expression and cellular susceptibility to SARS-CoV-2 infections in human kidney organoids and patient cells.Cell metabolism · 2022Article
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- SARS-CoV-2 infection and oxidative stress: Pathophysiological insight into thrombosis and therapeutic opportunities.Cytokine & growth factor reviews · 2022Review
- Reactive oxygen species, proinflammatory and immunosuppressive mediators induced in COVID-19: overlapping biology with cancer.RSC chemical biology · 2021Review
- Crosstalk of TLR4, vascular NADPH oxidase, and COVID-19 in diabetes: What are the potential implications?Vascular pharmacology · 2021Review
- Advances in use of mouse models to study the renin-angiotensin system.Molecular and cellular endocrinology · 2021Review
- Multifunctional angiotensin converting enzyme 2, the SARS-CoV-2 entry receptor, and critical appraisal of its role in acute lung injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Severe COVID-19: A multifaceted viral vasculopathy syndrome.Annals of diagnostic pathology · 2021Article
- Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19-Mechanisms and Therapeutic Targets.Oxidative medicine and cellular longevity · 2021Review
- Comparison of COVID-19 and Lung CancerFrontiers in oncology · 2021Review
- An update on ACE2 amplification and its therapeutic potential.Acta physiologica (Oxford, England) · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Abstract Angiotensin-converting enzyme 2 (ACE2) is highly expressed in the kidney and hydrolyzes angiotensin II (Ang II) to Ang(1-7). Since Ang II is a strong activator of oxidative stress, we reasoned that ACE2 could be involved in the regulation of renal oxidative stress by governing the levels of Ang II. We, therefore, assessed levels of oxidative stress in kidney cortex of ACE2 knockout and wild-type littermate mice under baseline conditions. We found multiple markers of increased oxidative stress in ACE2KO mice. NADPH oxidase activity was increased in kidney cortex from ACE2KO mice as compared to WT (227 ± 24% vs.100 ± 19%, P < 0.001). However, kidney catalase and superoxide dismutase activities were not different between groups. Exogenous Ang II was degraded less efficiently by kidneys from ACE2KO mice than WT mice, and administration of an AT1R blocker (losartan 30 mg/kg/day) resulted in normalization of NADPH oxidase activity in the ACE2KO. These findings suggest that an AT1R-dependent mechanism contributes to increased ROS observed in the ACE2KO. This study demonstrates that genetic deficiency of ACE2 activity in mice fosters oxidative stress in the kidney in the absence of overt hypertension and is associated with reduced kidney capacity to hydrolyze Ang II. ACE2KO mice serve as a novel in vivo model to examine the role of overactivity of NADPH oxidase in kidney function.
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Registered trials
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