Evidence map›Paper›PMID 20581171›Full record

ArticleAmerican journal of respiratory and critical care medicine2010

The angiotensin-converting enzyme 2/angiogenesis-(1-7)/Mas axis confers cardiopulmonary protection against lung fibrosis and pulmonary hypertension.

Vinayak Shenoy, Anderson J Ferreira, Yanfei Qi, Rodrigo A Fraga-Silva, Carlos Díez-Freire, Autumn Dooies, Joo Yun Jun, Srinivas Sriramula, Nithya Mariappan, Dorna Pourang and 7 more

Abstract readEvaluation Study
In one paragraph

Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.

0numbers the graph read from it
0cells of the map it votes in
157citing papers in PubMed
12.7field-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

157 citing papers in PubMed, 278 citations in OpenAlex.

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97 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

17 authors at 4 institutions in 3 countries.

Vinayak ShenoyDepartment of Pharmacodynamics, University of Florida, Gainesville, Florida, USA.
Anderson J Ferreira
Yanfei Qi
Rodrigo A Fraga-Silva
Carlos Díez-Freire
Autumn Dooies
Joo Yun Jun
Srinivas Sriramula
Nithya Mariappan
Dorna Pourang
Changaram S Venugopal
Joseph Francis
Timothy Reudelhuber
Robson A Santos
Jawaharlal M Patel
Mohan K Raizada
Michael J Katovich
Louisiana State University · USUniversity of Florida · USMontreal Clinical Research Institute · CAUniversidade Federal de Minas Gerais · BR

Funding

CVD protection mechanisms involving ACE2/Ang-(1-7) axisR01HL056921 · NHLBI · UNIVERSITY OF FLORIDA · PI RAIZADA, MOHAN K. · 1996 to 2015
$9.2M
NHLBI NIH HHS HL56921NHLBI NIH HHS R01 HL056921
6 · The paper itself

Abstract

rationaleAn activated vasoconstrictive, proliferative, and fibrotic axis of the renin angiotensin system (angiotensin-converting enzyme [ACE]/angiotensin [Ang]II/AngII type 1 receptor) has been implicated in the pathophysiology of pulmonary fibrosis (PF) and pulmonary hypertension (PH). The recent discovery of a counterregulatory axis of the renin angiotensin system composed of ACE2/Ang-(1-7)/Mas has led us to examine the role of this vasoprotective axis on such disorders.

objectivesWe hypothesized that Ang-(1-7) treatment would exert protective effects against PF and PH.

methodsLentiviral packaged Ang-(1-7) fusion gene or ACE2 cDNA was intratracheally administered into the lungs of male Sprague Dawley rats. Two weeks after gene transfer, animals received bleomycin (2.5 mg/kg). In a subsequent study, animals were administered monocrotaline (MCT, 50 mg/kg). MEASUREMENTS AND MAIN

resultsIn the PF study, bleomycin administration resulted in a significant increase in right ventricular systolic pressure, which was associated with the development of right ventricular hypertrophy. The lungs of these animals also exhibited excessive collagen deposition, decreased expression of ACE and ACE2, increased mRNA levels for transforming growth factor β and other proinflammatory cytokines, and increased protein levels of the AT₁R. Overexpression of Ang-(1-7) significantly prevented all the above-mentioned pathophysiological conditions. Similar protective effects were also obtained with ACE2 overexpression. In the PH study, rats injected with MCT developed elevated right ventricular systolic pressure, right ventricular hypertrophy, right ventricular fibrosis, and pulmonary vascular remodeling, all of which were attenuated by Ang-(1-7) overexpression. Blockade of the Mas receptor abolished the beneficial effects of Ang-(1-7) against MCT-induced PH.

conclusionsOur observations demonstrate a cardiopulmonary protective role for the ACE2/Ang-(1-7)/Mas axis in the treatment of lung disorders.

Indexed as

Genetic TherapyRenin-Angiotensin SystemAngiotensin-Converting Enzyme 2Angiotensin IAnimalsBleomycinHypertension, PulmonaryMalePeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsPulmonary FibrosisRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)BleomycinPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID20581171
PMCPMC2970847
OpenAlexW2015945747

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.