Evidence map›Paper›PMID 21215698›Full record

ReviewCurrent opinion in pharmacology2011

ACE2, a promising therapeutic target for pulmonary hypertension.

Vinayak Shenoy, Yanfei Qi, Michael J Katovich, Mohan K Raizada

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

57 citing papers in PubMed, 101 citations in OpenAlex.

  1. Mesenchymal stem cell therapy for pulmonary hypertension: an update.Frontiers in bioengineering and biotechnology · 2025
    Review
  2. Article
  3. A cardiotoxicity-eliminated ACE2 variant as a pan-inhibitor against coronavirus cell invasion.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  4. Medicina (Kaunas, Lithuania) · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. A review of cardio-pulmonary microvascular dysfunction in pulmonary hypertension.American heart journal plus : cardiology research and practice · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Phytoconstituents from ten natural herbs as potent inhibitors of main protease enzyme of SARS-COV-2:Phytomedicine plus : international journal of phytotherapy and phytopharmacology · 2021
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
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  20. Review
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

4 authors at 1 institution in 1 country.

Vinayak ShenoyDepartment of Physiology and Functional Genomics, University of Florida, Gainesville, FL, USA.
Yanfei Qi
Michael J Katovich
Mohan K Raizada
University of Florida · US

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
ACE2 as a target for pulmonary hypertension therapeuticsRC1HL099980 · NHLBI · UNIVERSITY OF FLORIDA · PI GRANT, MARIA BARTOLOMEO, RAIZADA, MOHAN K. · 2009 to 2010
$982k
NHLBI NIH HHS HL102033NHLBI NIH HHS HL 99980NHLBI NIH HHS R01 HL056921NHLBI NIH HHS R01 HL102033NHLBI NIH HHS RC1 HL099980
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a chronic lung disease with poor diagnosis and limited therapeutic options. The currently available therapies are ineffective in improving the quality of life and reducing mortality rates. There exists a clear unmet medical need to treat this disease, which necessitates the discovery of novel therapeutic targets/agents for safe and successful therapy. An altered renin-angiotensin system (RAS) has been implicated as a causative factor in the pathogenesis of PAH. Angiotensin II (Ang II), a key effector peptide of the RAS, can exert deleterious effects on the pulmonary vasculature resulting in vasoconstriction, proliferation, and inflammation, all of which contribute to PAH development. Recently, a new member of the RAS, angiotensin converting enzyme 2 (ACE2), was discovered. This enzyme functions as a negative regulator of the angiotensin system by metabolizing Ang II to a putative protective peptide, angiotensin-(1-7). ACE2 is abundantly expressed in the lung tissue and emerging evidence suggests a beneficial role for this enzyme against lung diseases. In this review, we focus on ACE2 in relation to pulmonary hypertension and provide proof of principle for its therapeutic role in PAH.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsAnimalsCell ProliferationEndothelium, VascularHumansHypertension, PulmonaryInflammationMuscle, Smooth, VascularOxidative StressPeptidyl-Dipeptidase AVentricular RemodelingACE2 protein, humanAngiotensin-Converting Enzyme 2Angiotensin-Converting Enzyme InhibitorsPeptidyl-Dipeptidase A

Identifiers

PMID21215698
PMCPMC3075309
OpenAlexW2019819067

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.