Evidence map›Paper›PMID 26697172›Full record

ArticlePulmonary circulation2015

Dose-dependent, therapeutic potential of angiotensin-(1-7) for the treatment of pulmonary arterial hypertension.

Siegfried Breitling, Adrienn Krauszman, Richa Parihar, Thomas Walther, Mark K Friedberg, Wolfgang M Kuebler

Abstract read
In one paragraph

Article in Pulmonary circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

  1. Trial
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  5. Review
  6. Neurohormonal modulation in pulmonary arterial hypertension.The European respiratory journal · 2021
    Review
  7. Targeting ACE2 for COVID-19 Therapy: Opportunities and Challenges.American journal of respiratory cell and molecular biology · 2021
    Review
  8. Article
  9. Article
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  13. Article
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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

6 authors.

Siegfried BreitlingKeenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada ; Institute for Chemistry and Biochemistry, Freie Universität Berlin, Berlin, Germany.
Adrienn KrauszmanKeenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada ; Institute of Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Richa PariharKeenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada.
Thomas WaltherDepartment of Pharmacology and Therapeutics, School of Medicine, School of Pharmacy, University College Cork, Cork, Ireland.
Mark K FriedbergLabatt Family Heart Center, Division of Cardiology and Cardiovascular Surgery, Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada.
Wolfgang M KueblerKeenan Research Centre for Biomedical Science, St. Michael's Hospital, Toronto, Ontario, Canada ; Institute of Physiology, Charité-Universitätsmedizin Berlin, Berlin, Germany ; Departments of Surgery and Physiology, University of Toronto, Toronto, Ontario, Canada; and German Heart Institute Berlin, Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effects of the heptapeptide angiotensin-(1-7) (Ang-(1-7)), via its receptor Mas, oppose many of the effects of the classic angiotensin II signaling pathway, and pharmacological exploitation of this effect is currently actively pursued for a wide range of cardiovascular, neoplastic, or immunological disorders. On the basis of its vasodilatory and antiproliferative properties, Ang-(1-7) has consequentially also been proposed as a novel therapeutic strategy for the treatment of pulmonary arterial hypertension (PAH). In this study, we tested the effectiveness of Ang-(1-7) and its stable, cyclic analog cAng-(1-7) over a range of doses for their therapeutic potential in experimental PAH. In the monocrotaline (MCT) rat model of PAH, Ang-(1-7) or cAng-(1-7) were injected in doses of 30, 100, 300, or 900 μg kg(-1) day(-1), and effects on pulmonary hemodynamics and vascular remodeling were assessed. Five weeks after MCT injection, right ventricular systolic pressure (RVSP) was significantly reduced for 3 dose groups treated with Ang-(1-7) (100, 300, and 900 μg kg(-1) day(-1)) and for all dose groups treated with cAng-(1-7), as compared to untreated controls, yet the total reduction of RVSP was <50% at best and thus markedly lower than that with a positive treatment control with ambrisentan. Medial-wall thickness in pulmonary arterioles was only slightly reduced, without reaching significance, for any of the tested Ang-(1-7) compounds and doses. The reported moderate attenuation of PAH does not confirm the previously postulated high promise of this strategy, and the therapeutic usefulness of Ang-(1-7) may be limited in PAH relative to that in other cardiovascular diseases.

Indexed as

pulmonary hypertensionrenin-angiotensin systemvascular remodeling

Identifiers

PMID26697172
PMCPMC4671739

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.