The extended renin-angiotensin system: a promising target for traumatic brain injury therapeutics

Following injury, activation of angiotensin II type I receptor (AT1R) in various cell types can promote inflammation, generate reactive oxygen species, increase glial proliferation, and reduce cerebral blood flow – physiological responses with known ability to damage brain parenchyma (Villapol et al...

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Bibliographic Details
Published in:Neural regeneration research 2020-06, Vol.15 (6), p.1025-1026
Main Authors: Janatpour, Zachary, Symes, Aviva
Format: Article
Language:English
Subjects:
Angiotensin II
Angiotensins
Animal cognition
Blood pressure
Blood-brain barrier
Brain injuries
Brain research
Clinical trials
Cognitive ability
Death
Dementia
Disabilities
Drug therapy
Enzymes
Inflammation
Ligands
Mammals
Peer review
Peptides
Proteins
Renin-angiotensin system
Telmisartan
Therapeutics
Traumatic brain injury
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Summary:Following injury, activation of angiotensin II type I receptor (AT1R) in various cell types can promote inflammation, generate reactive oxygen species, increase glial proliferation, and reduce cerebral blood flow – physiological responses with known ability to damage brain parenchyma (Villapol et al., 2012, 2015). [...]it stands to reason that blockade or countersignaling of AT1R would reduce damage in the traumatic penumbra. [...]candesartan and losartan also mediate some actions through acting as PPARγ partial agonists (Villapol et al., 2012, 2015). [...]in addition to their ability to block deleterious effects of AT1R signaling after insult, ARBs likely combat the molecular sequelae of TBI through multiple pathways. Since both telmisartan and candesartan are approved to treat hypertension in the USA (by the Food and Drug Administration) and are typically well tolerated, they merit consideration for use in TBI clinical trials.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.270304