Evidence map›Paper›PMID 33935785›Full record

ArticleFrontiers in pharmacology2021

Luteolin Ameliorates Experimental Pulmonary Arterial Hypertension via Suppressing Hippo-YAP/PI3K/AKT Signaling Pathway.

Wanyun Zuo, Na Liu, Yunhong Zeng, Zhenghui Xiao, Keke Wu, Fan Yang, Biao Li, Qingqing Song, Yunbin Xiao, Qiming Liu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.9field-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

40 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
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  8. Review
  9. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Bioactive compound combinations fromFrontiers in pharmacology · 2025
    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

10 authors at 3 institutions in 1 country.

Wanyun ZuoDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Na LiuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Yunhong ZengDepartment of Cardiology, Hunan Children's Hospital, Hunan, China.
Zhenghui XiaoDepartment of Cardiology, Hunan Children's Hospital, Hunan, China.
Keke WuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Fan YangDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Biao LiDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Qingqing SongDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Yunbin XiaoDepartment of Cardiology, Hunan Children's Hospital, Hunan, China.
Qiming LiuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital of Central South University, Hunan, China.
Central South University · CNHunan Children's Hospital · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Luteolin is a flavonoid compound with a variety of pharmacological effects. In this study, we explored the effects of luteolin on monocrotaline (MCT) induced rat pulmonary arterial hypertension (PAH) and underlying mechanisms. A rat PAH model was generated through MCT injection. In this model, luteolin improved pulmonary vascular remodeling and right ventricular hypertrophy, meanwhile, luteolin could inhibit the proliferation and migration of pulmonary artery smooth muscle cells induced by platelet-derived growth factor-BB (PDGF-BB) in a dose-dependent manner. Moreover, our results showed that luteolin could downregulate the expression of LATS1 and YAP, decrease YAP nuclear localization, reduce the expression of PI3K, and thereby restrain the phosphorylation of AKT induced by PDGF-BB. In conclusion, luteolin ameliorated experimental PAH, which was at least partly mediated through suppressing HIPPO-YAP/PI3K/AKT signaling pathway. Therefore, luteolin might become a promising candidate for treatment of PAH.

Indexed as

akthippo-yapluteolinPI3KPulmonary arterial hypertension

Identifiers

PMID33935785
PMCPMC8082250
OpenAlexW3153216759

What OpenQuestion holds

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LicenceCC BY
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.