ArticleNeuropharmacology2014
Neuronal over-expression of ACE2 protects brain from ischemia-induced damage.
Article in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 96 citations in OpenAlex.
- Angiotensin‑converting enzyme 2 expression in human tumors: Implications for prognosis and therapy (Review).Oncology reports · 2025Review
- Expression of SARS-CoV-2 entry receptor ACE2 in human brain and its association with Alzheimer's disease and COVID-19.Molecular psychiatry · 2025Review
- Unlocking the neuroprotective potential of peptide nucleic acids 5 (PNA5) in neurological diseases: molecular mechanisms to therapeutic approaches.Metabolic brain disease · 2025Review
- Exosomal MiRNA Therapy for Central Nervous System Injury Diseases.Cellular and molecular neurobiology · 2024Review
- Unveiling the Interplay-Vitamin D and ACE-2 Molecular Interactions in Mitigating Complications and Deaths from SARS-CoV-2.Biology · 2024Review
- A Review on Neuroinflammatory Pathway Mediating Through Ang-II/AT1 Receptors and a Novel Approach for the Treatment of Cerebral Ischemia in Combination with ARB's and Ceftriaxone.Annals of neurosciences · 2024Review
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Understanding the role of nACE2 in neurogenic hypertension among COVID-19 patients.Hypertension research : official journal of the Japanese Society of Hypertension · 2022Review
- Compromised endothelial progenitor cell exosomal communication with endothelial cells in hypertension ischemia conditions.Frontiers in stroke · 2022Article
- A review of ischemic stroke in COVID-19: currently known pathophysiological mechanisms.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Review
- Angiotensin-(1-7) as a Potential Therapeutic Strategy for Delayed Cerebral Ischemia in Subarachnoid Hemorrhage.Frontiers in immunology · 2022Review
- The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy.Biomedicines · 2021Review
- Changes of coagulation function and risk of stroke in patients with COVID-19.Brain and behavior · 2021Article
- Ischemic Stroke: An Underestimated Complication of COVID-19.Aging and disease · 2021Article
- Therapeutic effects of exosomes from angiotensin-converting enzyme 2 - overexpressed endothelial progenitor cells on intracerebral hemorrhagic stroke.Brain hemorrhages · 2021Article
- Article
- Potential mechanisms of cerebrovascular diseases in COVID-19 patients.Journal of neurovirology · 2021Review
- Simultaneous cardio-cerebral infarction in the coronavirus disease pandemic era: A case series.Medicine · 2021Article
- Therapeutic Strategies to Protect the Central Nervous System against Shiga Toxin from EnterohemorrhagicCurrent neuropharmacology · 2021Article
- Role of Brain Arterial Remodeling in HIV-Associated Cerebrovascular Outcomes.Frontiers in neurology · 2021Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Angiotensin (Ang) II exaggerates cerebral injury in ischemic damage. Angiotensin-converting enzyme type 2 (ACE2) converts Ang II into Ang (1-7) and thus, may protect against the effects of Ang II. We hypothesized that neuronal ACE2 over-expression decreases ischemic stroke in mice with Ang II overproduction. Human renin and angiotensinogen double transgenic (RA) mice and RA mice with neuronal over-expression of ACE2 (SARA) were used for the study. The mean arterial pressure (MAP) was calculated from telemetry-recorded blood pressure (BP). SARA mice were infused peripherally with Norepinephrine to "clamp" the BP, or intracerebroventricularly-infused with a Mas receptor antagonist (A-779). Middle cerebral artery occlusion (MCAO) surgery was performed to induce permanent focal ischemic stroke. Cerebral blood flow (CBF) and neurological function were determined. Two days after surgery, brain samples were collected for various analyses. Results showed: 1) When compared to chronically hypertensive RA mice, SARA mice had lower basal MAP, less MCAO-induced infarct volume, and increased CBF, neurological function and cerebral microvascular density in the peri-infarct area; 2) These changes in SARA mice were not altered after MAP "clamping", but partially reversed by brain infusion of A-779; 3) Ang (1-7)/Ang II ratio, angiogenic factors, endothelial nitric oxide synthase (eNOS) expression and nitric oxide production were increased, whereas, NADPH oxidase subunits and reactive oxygen species were decreased in the brain of SARA mice. ACE2 protects brain from ischemic injury via the regulation of NADPH oxidase/eNOS pathways by changing Ang (1-7)/Ang II ratio, independently of MAP changes.
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