Evidence map›Paper›PMID 23652350›Full record

ArticleLung2013

ACE2 activation confers endothelial protection and attenuates neointimal lesions in prevention of severe pulmonary arterial hypertension in rats.

Gang Li, Yinglong Liu, Yaobin Zhu, Aijun Liu, Yulin Xu, Xiaofeng Li, Zhiqiang Li, Junwu Su, Lizhong Sun

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. The renin-angiotensin system in models of pulmonary arterial hypertension vs primary hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Review
  3. Review
  4. Article
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  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Linking ACE2 and angiotensin II to pulmonary immunovascular dysregulation in SARS-CoV-2 infection.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2020
    Article
  17. Review
  18. From ACE2 to COVID-19: A multiorgan endothelial disease.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2020
    Article
  19. SARS-CoV-2 and the possible connection to ERs, ACE2, and RAGE: Focus on susceptibility factors.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Review
  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

9 authors at 3 institutions in 2 countries.

Gang LiPediatric Cardiac Center, Beijing Anzhen Hospital, Capital Medical University, Beijing, China.
Yinglong Liu
Yaobin Zhu
Aijun Liu
Yulin Xu
Xiaofeng Li
Zhiqiang Li
Junwu Su
Lizhong Sun
Capital Medical University · CNCapital University · USBeijing Anzhen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAngiotensin-converting enzyme 2 (ACE2), an ACE homolog, hydrolyzes angiotensin II and opposes its actions, and plays a protective role in the pathogenesis of pulmonary arterial hypertension (PAH). However, the underlying mechanisms involved in the effect of ACE2 on PAH are still uncertain. In this study, we observed the effects of ACE2 activation on endothelial dysfunction and vascular remodeling in the development of severe PAH in rats.

methodsSevere PAH was induced by monocrotaline injection 1 week following left pneumonectomy, and ACE2 was activated by continuous injection of resorcinolnaphthalein. The PAH-related hemodynamics, pathological changes, and endothelium-dependent vasorelaxation were examined to assess the effects of ACE2 activation. In addition, the changes of the main components of the renin-angiotensin system were identified by ELISA or Western blotting.

resultsSevere PAH was established at 3 weeks and was characterized by high pulmonary arterial pressure (45 mmHg), significant right ventricular hypertrophy, neointimal occlusive lesions, and impaired endothelium-dependent relaxation in pulmonary arteries. Coadministration of resorcinolnaphthalein reduced pulmonary arterial pressure, right ventricular hypertrophy, and neointimal formation and shifted the endothelial-dependent responses toward values measured in normal rats. Theses changes were associated with an increase in ACE2 and angiotensin-(1-7) levels and a decrease in ACE and angiotensin II levels, in addition to a decrease in the ACE/ACE2 ratio and the angiotensin II/angiotensin-(1-7) ratio. The beneficial effects of resorcinolnaphthalein were abolished by A-779.

conclusionsThese findings suggested that ACE2 activation by resorcinolnaphthalein improved endothelial function and suppressed neointimal formation in the prevention of severe PAH by the mechanism of mediating the levels of the components of the renin-angiotensin system.

Indexed as

Angiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAnimalsArterial PressureCytoprotectionDisease Models, AnimalEndothelium, VascularEnzyme ActivationEnzyme ActivatorsFamilial Primary Pulmonary HypertensionHypertension, PulmonaryHypertrophy, Right VentricularMaleMonocrotalineNaphthalenesAce2 protein, ratAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIEnzyme ActivatorsMonocrotalinenaphthaleneNaphthalenesPeptide FragmentsPeptidyl-Dipeptidase AresorcinolResorcinols

Identifiers

PMID23652350
OpenAlexW2061564804

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.