Evidence map›Paper›PMID 40962402›Full record

ReviewEuropean respiratory review : an official journal of the European Respiratory Society2025

SOX17 in pulmonary arterial hypertension: from development to clinical phenotype.

Thomas Lacoste-Palasset, Benoit Aguado, Julien Grynblat, Florence Coulet, Marc Humbert, Fabrice Antigny, David Montani, Grégoire Ruffenach

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in European respiratory review : an official journal of the European Respiratory Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Thomas Lacoste-PalassetUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.
Benoit AguadoUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.
Julien GrynblatUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.
Florence CouletSorbonne Université, Département de génétique médicale, Assistance Publique-Hôpitaux de Paris, Hôpital Pitié-Salpêtrière, Paris, France.ORCID https://orcid.org/0000-0002-5325-5272
Marc HumbertUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.ORCID https://orcid.org/0000-0003-0703-2892
Fabrice AntignyUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.ORCID https://orcid.org/0000-0002-9515-6571
David MontaniUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France.ORCID https://orcid.org/0000-0002-9358-6922
Grégoire RuffenachUniversité Paris-Saclay, INSERM, UMR_S 999, Hypertension Pulmonaire: Physiopathologie and Innovation Thérapeutique (HPPIT), AP-HP, Hôpital Bicêtre, Hôpital Marie Lannelongue (Groupe Hospitalier Paris Saint Joseph), ERN-LUNG, Le Plessis Robinson, France gregoire.ruffenach@inserm.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe disease characterised by progressive remodelling and loss of pulmonary microvessels, driven by endothelial cell dysfunction, smooth muscle cell abnormalities, inflammation and immune system dysregulation. Recent research advancements have uncovered pathogenic rare loss-of-function variants of

Indexed as

Arterial PressureHMGB ProteinsHypertension, PulmonaryPulmonary Arterial HypertensionPulmonary ArterySOXF Transcription FactorsAnimalsGenetic Predisposition to DiseaseHumansPhenotypePrognosisSignal TransductionVascular RemodelingHMGB ProteinsSOX17 protein, humanSOXF Transcription Factors

Identifiers

PMID40962402
PMCPMC12441814

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.