Evidence map›Paper›PMID 26322922›Full record

ReviewJournal of cardiovascular pharmacology2015

ACE2 and Microbiota: Emerging Targets for Cardiopulmonary Disease Therapy.

Colleen T Cole-Jeffrey, Meng Liu, Michael J Katovich, Mohan K Raizada, Vinayak Shenoy

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

64 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Microorganisms · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. When the clock ticks wrong with COVID-19.Clinical and translational medicine · 2022
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Article

4 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

5 authors.

Colleen T Cole-JeffreyDepartments of *Physiology and Functional Genomics; and †Pharmacodynamics, Colleges of Medicine and Pharmacy, University of Florida, Gainesville, FL.
Meng Liu
Michael J Katovich
Mohan K Raizada
Vinayak Shenoy

Funding

CVD protection mechanisms involving ACE2/Ang-(1-7) axisR01HL056921 · NHLBI · UNIVERSITY OF FLORIDA · PI RAIZADA, MOHAN K. · 1996 to 2015
$9.2M
Angiotensin-Converting Enzyme2 in Vascular Endothelial FunctionR01HL102033 · NHLBI · UNIVERSITY OF FLORIDA · PI RAIZADA, MOHAN K. · 2010 to 2019
$4.3M
NHLBI NIH HHS HL 056921NHLBI NIH HHS HL 102033NHLBI NIH HHS R01 HL056921NHLBI NIH HHS R01 HL102033
6 · The paper itself

Abstract

The health of the cardiovascular and pulmonary systems is inextricably linked to the renin-angiotensin system (RAS). Physiologically speaking, a balance between the vasodeleterious (Angiotensin-converting enzyme [ACE]/Angiotensin II [Ang II]/Ang II type 1 receptor [AT1R]) and vasoprotective (Angiotensin-converting enzyme 2 [ACE2]/Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor [MasR]) components of the RAS is critical for cardiopulmonary homeostasis. Upregulation of the ACE/Ang II/AT1R axis shifts the system toward vasoconstriction, proliferation, hypertrophy, inflammation, and fibrosis, all factors that contribute to the development and progression of cardiopulmonary diseases. Conversely, stimulation of the vasoprotective ACE2/Ang-(1-7)/MasR axis produces a counter-regulatory response that promotes cardiovascular health. Current research is investigating novel strategies to augment actions of the vasoprotective RAS components, particularly ACE2, in order to treat various pathologies. Although multiple approaches to increase the activity of ACE2 have displayed beneficial effects against experimental disease models, the mechanisms behind its protective actions remain incompletely understood. Recent work demonstrating a non-catalytic role for ACE2 in amino acid transport in the gut has led us to speculate that the therapeutic effects of ACE2 can be mediated, in part, by its actions on the gastrointestinal tract and/or gut microbiome. This is consistent with emerging data which suggest that dysbiosis of the gut and lung microbiomes is associated with cardiopulmonary disease. This review highlights new developments in the protective actions of ACE2 against cardiopulmonary disorders, discusses innovative approaches to targeting ACE2 for therapy, and explores an evolving role for gut and lung microbiota in cardiopulmonary health.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsCardiovascular AgentsDrug Delivery SystemsHeart DiseasesHumansLung DiseasesMicrobiotaPeptidyl-Dipeptidase APolymorphism, GeneticProto-Oncogene MasACE2 protein, humanAngiotensin-Converting Enzyme 2Cardiovascular AgentsMAS1 protein, humanPeptidyl-Dipeptidase AProto-Oncogene Mas

Identifiers

PMID26322922
PMCPMC4807023

What OpenQuestion holds

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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.