ArticleHypertension (Dallas, Tex. : 1979)2015
Activation of the Neuroprotective Angiotensin-Converting Enzyme 2 in Rat Ischemic Stroke.
Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 65 citations in OpenAlex.
- Activation of Angiotensin-Converting Enzyme 2 Mitigates Gastrointestinal Acute Radiation Syndrome.International journal of radiation oncology, biology, physics · 2026Article
- Diminazene Alleviates Neuroinflammation in Ischemic Stroke by Inhibiting Astrocytic Endoplasmic Reticulum Stress and Oxidative Stress.Neurochemical research · 2025Article
- Diminazene Aceturate (DIZE) Ameliorates Hypertension and Induces Anxiolytic- and Antidepressant-like Effects in TGR(mRen2)27.Protein and peptide letters · 2025Article
- ACE2 Rescues Sepsis-Associated Encephalopathy by Reducing Inflammation, Oxidative Stress, and Neuronal Apoptosis via the Nrf2/Sestrin2 Signaling Pathway.Molecular neurobiology · 2024Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Inhibition of the postsynaptic density protein 95 on the protective effect of Ang-(1-7)-Mas on cerebral ischaemia injury.Stroke and vascular neurology · 2022Article
- Is Diminazene an Angiotensin-Converting Enzyme 2 (ACE2) Activator? Experimental Evidence and Implications.The Journal of pharmacology and experimental therapeutics · 2022Article
- Mitigation of Multi-Organ Radiation Injury with ACE2 Agonist Diminazene Aceturate.Radiation research · 2022Article
- Angiotensin-(1-7) as a Potential Therapeutic Strategy for Delayed Cerebral Ischemia in Subarachnoid Hemorrhage.Frontiers in immunology · 2022Review
- Controlled Hemorrhage Sensitizes Angiotensin II-Elicited Hypertension through Activation of the Brain Renin-Angiotensin System Independently of Endoplasmic Reticulum Stress.Oxidative medicine and cellular longevity · 2022Article
- The Role of the ACE2/MasR Axis in Ischemic Stroke: New Insights for Therapy.Biomedicines · 2021Review
- Human placenta mesenchymal stem cell protection in ischemic stroke is angiotensin converting enzyme-2 and masR receptor-dependent.Stem cells (Dayton, Ohio) · 2021Article
- Stroke increases the expression of ACE2, the SARS-CoV-2 binding receptor, in murine lungs.Brain, behavior, and immunity · 2021Article
- The counter regulatory axis of the renin angiotensin system in the brain and ischaemic stroke: Insight from preclinical stroke studies and therapeutic potential.Cellular signalling · 2020Review
- Article
- Peptidase neurolysin functions to preserve the brain after ischemic stroke in male mice.Journal of neurochemistry · 2020Article
- Article
- Stimulation of the ACE2/Ang-(1-7)/Mas axis in hypertensive pregnant rats attenuates cardiovascular dysfunction in adult male offspring.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- β-Cyclodextrin as a Functional Excipient Used for Enhancing the Diminazene Aceturate Bioavailability.Pharmaceutics · 2019Article
- Revisiting the Brain Renin-Angiotensin System-Focus on Novel Therapies.Current hypertension reports · 2019Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas axis represents a promising target for inducing stroke neuroprotection. Here, we explored stroke-induced changes in expression and activity of endogenous angiotensin-converting enzyme 2 and other system components in Sprague-Dawley rats. To evaluate the clinical feasibility of treatments that target this axis and that may act in synergy with stroke-induced changes, we also tested the neuroprotective effects of diminazene aceturate, an angiotensin-converting enzyme 2 activator, administered systemically post stroke. Among rats that underwent experimental endothelin-1-induced ischemic stroke, angiotensin-converting enzyme 2 activity in the cerebral cortex and striatum increased in the 24 hours after stroke. Serum angiotensin-converting enzyme 2 activity was decreased within 4 hours post stroke, but rebounded to reach higher than baseline levels 3 days post stroke. Treatment after stroke with systemically applied diminazene resulted in decreased infarct volume and improved neurological function without apparent increases in cerebral blood flow. Central infusion of A-779, a Mas receptor antagonist, resulted in larger infarct volumes in diminazene-treated rats, and central infusion of the angiotensin-converting enzyme 2 inhibitor MLN-4760 alone worsened neurological function. The dynamic alterations of the protective angiotensin-converting enzyme 2 pathway after stroke suggest that it may be a favorable therapeutic target. Indeed, significant neuroprotection resulted from poststroke angiotensin-converting enzyme 2 activation, likely via Mas signaling in a blood flow-independent manner. Our findings suggest that stroke therapeutics that target the angiotensin-converting enzyme 2/angiotensin-(1-7)/Mas axis may interact cooperatively with endogenous stroke-induced changes, lending promise to their further study as neuroprotective agents.
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Registered trials
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.