Evidence map›Paper›PMID 39125817›Full record

ArticleInternational journal of molecular sciences2024

Urolithin A Protects against Hypoxia-Induced Pulmonary Hypertension by Inhibiting Pulmonary Arterial Smooth Muscle Cell Pyroptosis via AMPK/NF-κB/NLRP3 Signaling.

Xinjie He, Zhinan Wu, Jinyao Jiang, Wenyi Xu, Ancai Yuan, Fei Liao, Song Ding, Jun Pu

Abstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. NF-κB and pulmonary hypertension: Advances in mechanistic research and therapeutic applications.American heart journal plus : cardiology research and practice · 2025
    Review
  8. Review
  9. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
    Review
  10. Review
  11. [Application of Animal Models in Research on Hypoxia-Related Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025
    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

8 authors.

Xinjie HeDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Zhinan WuDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Jinyao JiangDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Wenyi XuDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.ORCID 0000-0002-6588-675X
Ancai YuanDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Fei LiaoDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Song DingDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
Jun PuDepartment of Cardiology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.

Funding

National Natural Science Foundation of China 82070477National Natural Science Foundation of China 82370475Shanghai Science and Technology Committee 22XD1421800
6 · The paper itself

Abstract

Recent studies confirmed that pyroptosis is involved in the progression of pulmonary hypertension (PH), which could promote pulmonary artery remodeling. Urolithin A (UA), an intestinal flora metabolite of ellagitannins (ETs) and ellagic acid (EA), has been proven to possess inhibitory effects on pyroptosis under various pathological conditions. However, its role on PH remained undetermined. To investigate the potential of UA in mitigating PH, mice were exposed to hypoxia (10% oxygen, 4 weeks) to induce PH, with or without UA treatment. Moreover, in vitro experiments were carried out to further uncover the underlying mechanisms. The in vivo treatment of UA suppressed the progression of PH via alleviating pulmonary remodeling. Pyroptosis-related genes were markedly upregulated in mice models of PH and reversed after the administration of UA. In accordance with that, UA treatment significantly inhibited hypoxia-induced pulmonary arterial smooth muscle cell (PASMC) pyroptosis via the AMPK/NF-κB/NLRP3 pathway. Our results revealed that UA treatment effectively mitigated PH progression through inhibiting PASMC pyroptosis, which represents an innovative therapeutic approach for PH.

Indexed as

AMP-Activated Protein KinasesCoumarinsHypertension, PulmonaryHypoxiaMyocytes, Smooth MuscleNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinPulmonary ArteryPyroptosisSignal TransductionAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BL3,8-dihydroxy-6H-dibenzo(b,d)pyran-6-oneAMP-Activated Protein KinasesCoumarinsNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinAMPKpulmonary hypertensionpulmonary smooth muscle cellspyroptosisUrolithin A

Identifiers

PMID39125817
PMCPMC11311380

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.