Evidence map›Paper›PMID 24102099›Full record

ReviewClinical science (London, England : 1979)2014

Cerebroprotective action of angiotensin peptides in stroke.

Robert W Regenhardt, Douglas M Bennion, Colin Sumners

Open access · greenAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 3 pooled it
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  8. Review
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  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Care for Patients with Stroke During the COVID-19 Pandemic: Physical Therapy and Rehabilitation Suggestions for Preventing Secondary Stroke.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Robert W Regenhardt*Department of Physiology and Functional Genomics and McKnight Brain Institute, University of Florida, 1600 SW Archer Road, PO Box 100274, Gainesville, FL 32610-0274, U.S.A.
Douglas M Bennion
Colin Sumners
University of Florida · US

Funding

Multidisciplinary Training Program in HypertensionT32HL083810 · NHLBI · UNIVERSITY OF FLORIDA · PI WOOD, CHARLES E · 2007 to 2017
$2.5M
NHLBI NIH HHS T32 HL083810
6 · The paper itself

Abstract

The goal of the present review is to examine the evidence for beneficial actions of manipulation of the RAS (renin-angiotensin system) in stroke, with particular focus on Ang-(1-7) [angiotensin-(1-7)] and its receptor Mas. The RAS appears to be highly involved in the multifactorial pathophysiology of stroke. Blocking the effects of AngII (angiotensin II) at AT1R (AngII type 1 receptor), through the use of commonly prescribed ACE (angiotensin-converting enzyme) inhibitors or AT1R blockers, has been shown to have therapeutic effects in both ischaemic and haemorrhagic stroke. In contrast with the deleterious actions of over activation of AT1R by AngII, stimulation of AT2Rs (AngII type 2 receptors) in the brain has been demonstrated to elicit beneficial effects in stroke. Likewise, the ACE2/Ang-(1-7)/Mas axis of the RAS has been shown to have therapeutic effects in stroke when activated, countering the effects of the ACE/AngII/AT1R axis. Studies have demonstrated that activating this axis in the brain elicits beneficial cerebral effects in rat models of ischaemic stroke, and we have also demonstrated the cerebroprotective potential of this axis in haemorrhagic stroke using stroke-prone spontaneously hypertensive rats and collagenase-induced striatal haemorrhage. The mechanism of cerebroprotection elicited by ACE2/Ang-(1-7)/Mas activation includes anti-inflammatory effects within the brain parenchyma. The major hurdle to overcome in translating these results to humans is devising strategies to activate the ACE2/Ang-(1-7)/Mas cerebroprotective axis using post-stroke treatments that can be administered non-invasively.

Indexed as

Angiotensin IAnimalsHumansPeptide FragmentsPeptidesProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledRenin-Angiotensin SystemStrokeTranslational Research, BiomedicalVasodilator AgentsAngiotensin Iangiotensin I (1-7)Peptide FragmentsPeptidesProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledVasodilator Agents

Identifiers

PMID24102099
PMCPMC7453725
OpenAlexW1978607907

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.