Evidence map›Paper›PMID 25337184›Full record

ArticleInternational journal of clinical and experimental pathology2014

Triggering the succinate receptor GPR91 enhances pressure overload-induced right ventricular hypertrophy.

Lei Yang, Di Yu, Huan-Huan Fan, Yu Feng, Liang Hu, Wei-Yan Zhang, Kai Zhou, Xu-Ming Mo

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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  5. Metabolite signaling in the heart.Nature cardiovascular research · 2023
    Review
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  8. Cardioprotection in right heart failure.British journal of pharmacology · 2020
    Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. 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

8 authors at 2 institutions in 1 country.

Lei YangDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Di YuDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Huan-Huan FanDepartment of Gynaecology, Jiangsu Province Hospital of TCM Jiangsu Province, China.
Yu FengDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Liang HuDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Wei-Yan ZhangDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Kai ZhouDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Xu-Ming MoDepartment of Cardiothoracic Surgery, Nanjing Children's Hospital Affiliated of Nanjing Medical University Jiangsu Province, China.
Nanjing Children's Hospital · CNJiangsu Province Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPulmonary arterial hypertension (PAH) leads to pressure overload in the right ventricle (RV) and induces right ventricular hypertrophy (RVH). GPR91 is an orphan G-protein-coupled receptor (GPCR) that has been characterized as a receptor for succinate, which increases in RVH; however, its role remains unknown. METHODS AND

resultsWe studied succinate-GPR91 signaling in a pulmonary arterial banding (PAB) model of RVH in the SD rats due to pressure overload. We report that GPR91 was located in cardiomyocytes. We found that the expressions of GPR91 and p-Akt in the RV significantly increased in the PAB model compared with the sham. In the PAB rats, the treatment of succinate further increased the p-Akt levels and aggravated RVH in vivo. In in vitro studies, succinate stimulated the up-regulation of the hypertrophic gene marker anp. All these effects were inhibited by the antagonist of PI3K, wortmannin, both in vivo and in vitro. Finally, we found that the GPR91-PI3K/Akt axis was also up-regulated compared with the sham in human RVH.

conclusionsOur results suggest that succinate-GPR91 is involved in RVH via PI3K/Akt signaling in vivo and in vitro. GPR91 may be a novel therapeutic target for RVH induced by pressure overload.

Indexed as

AnimalsAtrial Natriuretic FactorCells, CulturedDisease Models, AnimalHypertension, PulmonaryHypertrophy, Right VentricularMaleMyocytes, CardiacPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-aktRats, Sprague-DawleyReceptors, G-Protein-CoupledRNA InterferenceAtrial Natriuretic FactorPhosphatidylinositol 3-KinasePhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, G-Protein-CoupledSuccinic AcidSucnr1 protein, ratPI3K/Aktright ventricular hypertrophySuccinate G-protein-receptor 91

Identifiers

PMID25337184
PMCPMC4203155
OpenAlexW275844747

What OpenQuestion holds

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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.