Evidence map›Paper›PMID 30443713›Full record

ReviewNeurochemical research2019

ACE2 in Brain Physiology and Pathophysiology: Evidence from Transgenic Animal Models.

Natalia Alenina, Michael Bader

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurochemical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 5 pooled it
14.5field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 5 syntheses or guidelines pooled it, 139 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Impact of Cardiovascular Diseases on COVID-19: A Systematic Review.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Pooled it
  4. Renal Injury by SARS-CoV-2 Infection: A Systematic Review.Kidney diseases (Basel, Switzerland) · 2021
    Pooled it
  5. Intracranial hemorrhage in coronavirus disease 2019 (COVID-19) patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Pooled it
  6. Article
  7. Microglial activation and RAS signaling: a dual-edged sword in neuroinflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  8. Article
  9. ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Natalia AleninaMax-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, 13125, Berlin, Germany.
Michael BaderMax-Delbrück-Center for Molecular Medicine (MDC), Robert-Rössle-Str. 10, 13125, Berlin, Germany. mbader@mdc-berlin.de.ORCID http://orcid.org/0000-0003-4780-4164
Max Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin-converting enzyme 2 (ACE2) is a protein consisting of two domains, the N-terminus is a carboxypeptidase homologous to ACE and the C-terminus is homologous to collectrin and responsible for the trafficking of the neutral amino acid transporter B(0)AT1 to the plasma membrane of gut epithelial cells. The carboxypeptidase domain not only metabolizes angiotensin II to angiotensin-(1-7), but also other peptide substrates, such as apelin, kinins and morphins. In addition, the collectrin domain regulates the levels of some amino acids in the blood, in particular of tryptophan. Therefore it is of no surprise that animals with genetic alterations in the expression of ACE2 develop a diverse pattern of phenotypes ranging from hypertension, metabolic and behavioural dysfunctions, to impairments in serotonin synthesis and neurogenesis. This review summarizes the phenotypes of such animals with a particular focus on the central nervous system.

Indexed as

PhenotypeAngiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAnimalsAnimals, Genetically ModifiedBrainBrain DiseasesCardiomegalyModels, AnimalPeptide FragmentsPeptidyl-Dipeptidase ASerotoninStress, PsychologicalTryptophanAce2 protein, mouseAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIPeptide FragmentsPeptidyl-Dipeptidase ASerotoninTryptophanAngiotensinHypertensionKnockout miceSARSSerotoninTransgenic mice

Identifiers

PMID30443713
PMCPMC7089194
OpenAlexW2901216321

What OpenQuestion holds

Textmetadata
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.