ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2014
Angiotensin receptor type 2 activation induces neuroprotection and neurogenesis after traumatic brain injury.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.
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Who cites it
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- Comparative effects of angiotensin II stimulating and inhibiting antihypertensives on dementia risk: a systematic review and meta-analysis.GeroScience · 2025Pooled it
- A Systematic Review of Closed Head Injury Models of Mild Traumatic Brain Injury in Mice and Rats.Journal of neurotrauma · 2019Pooled it
- Neuronal Injury and Regeneration-Linked Gene Expression Dynamics in the Hypothalamic-Pituitary-Adrenal Axis Following Experimental Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Ang II-mediated effects on BBB integrity in psychiatric and neurological disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2026Review
- Neuroprotective effects of candesartan in 3-nitropropionic acid-induced Huntington's disease: modulation of angiotensin and CREB/BDNF/PGC1-α signaling.Inflammopharmacology · 2025Article
- Characterization of Neurensin-2 knockout mice: insights into stress-resilience mechanisms.Translational psychiatry · 2025Article
- Renin-angiotensin system as an emerging target to modulate adult neurogenesis in health and disease.Stem cell research & therapy · 2025Review
- Enhancing glymphatic transport through angiotensin II type 2 receptor activation promotes neurological recovery after traumatic brain injury.Theranostics · 2025Article
- The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Review
- Article
- The Angiotensin ATPharmacological reviews · 2022Review
- AT2 activation does not influence brain damage in the early phase after experimental traumatic brain injury in male mice.Scientific reports · 2022Article
- Manifestation of renin angiotensin system modulation in traumatic brain injury.Metabolic brain disease · 2021Review
- The Role of BDNF in Experimental and Clinical Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- The role of peptidase neurolysin in neuroprotection and neural repair after stroke.Neural regeneration research · 2021Article
- The Brain AT2R-a Potential Target for Therapy in Alzheimer's Disease and Vascular Cognitive Impairment: a Comprehensive Review of Clinical and Experimental Therapeutics.Molecular neurobiology · 2020Review
- The extended renin-angiotensin system: a promising target for traumatic brain injury therapeutics.Neural regeneration research · 2020Review
- Article
- Angiotensin II Receptor 1 Blockage Limits Brain Damage and Improves Functional Outcome After Brain Injury in Aged Animals Despite Age-Dependent Reduction in AT1 Expression.Frontiers in aging neuroscience · 2019Article
- Stem cells technology: a powerful tool behind new brain treatments.Drug delivery and translational research · 2018Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiotensin II receptor type 2 (AT(2)) agonists have been shown to limit brain ischemic insult and to improve its outcome. The activation of AT(2) was also linked to induced neuronal proliferation and differentiation in vitro. In this study, we examined the therapeutic potential of AT(2) activation following traumatic brain injury (TBI) in mice, a brain pathology that displays ischemia-like secondary damages. The AT(2) agonist CGP42112A was continuously infused immediately after closed head injury (CHI) for 3 days. We have followed the functional recovery of the injured mice for 35 days post-CHI, and evaluated cognitive function, lesion volume, molecular signaling, and neurogenesis at different time points after the impact. We found dose-dependent improvement in functional recovery and cognitive performance after CGP42112A treatment that was accompanied by reduced lesion volume and induced neurogenesis in the neurogenic niches of the brain and also in the injury region. At the cellular/molecular level, CGP42112A induced early activation of neuroprotective kinases protein kinase B (Akt) and extracellular-regulated kinases ½ (ERK½), and the neurotrophins nerve growth factor and brain-derived neurotrophic factor; all were blocked by treatment with the AT(2) antagonist PD123319. Our results suggest that AT(2) activation after TBI promotes neuroprotection and neurogenesis, and may be a novel approach for the development of new drugs to treat victims of TBI.
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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.