Evidence map›Paper›PMID 31573044›Full record

ArticleInternational journal of molecular medicine2019

Protective effect of hydrogen sulfide on monocrotaline‑induced pulmonary arterial hypertension via inhibition of the endothelial mesenchymal transition.

Hui Zhang, Yanjun Lin, Yiwen Ma, Junfeng Zhang, Changqian Wang, Huili Zhang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Genetic Delivery and Gene Therapy in Pulmonary Hypertension.International journal of molecular sciences · 2021
    Review
  16. Article
  17. Article
  18. Review
  19. 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

6 authors at 1 institution in 1 country.

Hui ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Yanjun LinDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Yiwen MaDepartment of Anesthesiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Junfeng ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Changqian WangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Huili ZhangDepartment of Cardiology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China.
Shanghai Ninth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial‑to‑mesenchymal transition (EndMT) serves an important role in the vascular remodeling of pulmonary arterial hypertension (PAH). However, little is known about the correlation between hydrogen sulfide (H2S), a protective gaseous mediator in PAH and the process of EndMT. Male Sprague‑Dawley rats (10 weeks old) received a single dose of monocrotaline (MCT; i.p., 60 mg/kg) and were randomly treated with NaHS [an H2S donor; intraperitoneal (i.p.) 1 mg/kg/day], DL‑propagylglycine (an inhibitor of H2S synthesis; PAG; i.p., 10 mg/kg/day) or saline, 7 days after MCT injection. Rats were sacrificed 21 days after MCT injection. A selection of human pulmonary artery endothelial cells (HPAECs) were pretreated with NaHS or saline and stimulated with transforming growth factor (TGF)‑β1 (10 ng/ml), and the other HPAECs were transfected with a cystathionine γ‑lyase (CSE, an H2S synthesizing enzyme) plasmid and subsequently stimulated with TGF‑β1. NaHS was indicated to inhibit EndMT and PAH progression by inhibiting the induction of the nuclear factor (NF)‑κB‑Snail pathway. In contrast, the depletion of H2S formation by PAG exacerbated EndMT and PAH by activating NF‑κB‑Snail molecules. In HPAECs, NaHS dose‑dependently inhibited TGF‑β1‑induced EndMT and the activation of the NF‑κB‑Snail pathway. Transfection with a CSE plasmid significantly repressed TGF‑β1‑induced expression of the mesenchymal marker and upregulated the expression of the endothelial marker, which was accompanied by the suppression of the NF‑κB‑Snail pathway. The inhibitory effect of CSE overexpression on TGF‑β1‑induced EndMT was significantly reversed by pretreatment with PAG. In conclusion, the current study provides novel information elucidating the beneficial effect of H2S on PAH through inhibiting the induction of the NF‑κB‑Snail pathway and the subsequent process of EndMT in pulmonary arteries.

Indexed as

AnimalsEndothelial CellsGlycineHumansHydrogen SulfideMonocrotalineNF-kappa BPulmonary Arterial HypertensionPulmonary ArteryRatsSignal TransductionSnail Family Transcription FactorsTransforming Growth Factor beta1Vascular RemodelingDL-propagylglycineGlycineHydrogen SulfideMonocrotalineNF-kappa BSNAI1 protein, humanSnail Family Transcription FactorsTGFB1 protein, humanTransforming Growth Factor beta1

Identifiers

PMID31573044
PMCPMC6844600
OpenAlexW2978080892

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.