Evidence map›Paper›PMID 38841857›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2024

Molecular Changes Implicate Angiogenesis and Arterial Remodeling in Systemic Sclerosis-Associated and Idiopathic Pulmonary Hypertension.

Yuechen Zhou, Tracy Tabib, Mengqi Huang, Ke Yuan, Yunhye Kim, Christina Morse, John Sembrat, Eleanor Valenzi, Robert Lafyatis

Abstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Endothelial Heterogeneity in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. 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

9 authors.

Yuechen ZhouDivision of Rheumatology and Clinical Immunology (Y.Z., T.T., M.H., C.M., R.L.), University of Pittsburgh, PA.
Tracy TabibDivision of Rheumatology and Clinical Immunology (Y.Z., T.T., M.H., C.M., R.L.), University of Pittsburgh, PA.ORCID 0000-0003-4053-988X
Mengqi HuangDivision of Rheumatology and Clinical Immunology (Y.Z., T.T., M.H., C.M., R.L.), University of Pittsburgh, PA.ORCID 0000-0002-1675-8575
Ke YuanDivision of Pulmonary Medicine, Boston Children's Hospital and Harvard Medical School, MA (K.Y., Y.K.).
Yunhye KimDivision of Pulmonary Medicine, Boston Children's Hospital and Harvard Medical School, MA (K.Y., Y.K.).ORCID 0009-0002-1804-571X
Christina MorseDivision of Rheumatology and Clinical Immunology (Y.Z., T.T., M.H., C.M., R.L.), University of Pittsburgh, PA.ORCID 0000-0002-5744-0512
John SembratDivision of Pulmonary, Allergy and Critical Care Medicine (J.S., E.V.), University of Pittsburgh, PA.ORCID 0000-0003-4108-803X
Eleanor ValenziDivision of Pulmonary, Allergy and Critical Care Medicine (J.S., E.V.), University of Pittsburgh, PA.
Robert LafyatisDivision of Rheumatology and Clinical Immunology (Y.Z., T.T., M.H., C.M., R.L.), University of Pittsburgh, PA.ORCID 0000-0002-9398-5034

Funding

Systems Biology CoreP50AR080612 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROBERT A. LAFYATIS · 2022 to 2026
$9.5M
NIAMS NIH HHS P50 AR080612
6 · The paper itself

Abstract

backgroundPulmonary hypertension (PH) is a common complication of systemic sclerosis (SSc) and a leading cause of mortality among patients with this disease. PH can also occur as an idiopathic condition (idiopathic pulmonary arterial hypertension). Investigation of transcriptomic alterations in vascular populations is critical to elucidating cellular mechanisms underlying pathobiology of SSc-associated and idiopathic PH.

methodsWe analyzed single-cell RNA sequencing profiles of endothelial and perivascular mesenchymal populations from explanted lung tissue of patients with SSc-associated PH (n=16), idiopathic pulmonary arterial hypertension (n=3), and healthy controls (n=15). Findings were validated by immunofluorescence staining of explanted human lung tissue.

resultsThree disease-associated endothelial populations emerged. Two angiogenic endothelial cell (EC) subtypes markedly expanded in SSc-associated PH lungs: tip ECs expressing canonical tip markers

conclusionsThese data provide high-resolution insights into the complexity and plasticity of the pulmonary endothelium in SSc-associated PH and idiopathic pulmonary arterial hypertension and provide direct molecular insights into soluble mediators and transcription factors driving PH vasculopathy.

Indexed as

Neovascularization, PathologicScleroderma, SystemicVascular RemodelingAdultAngiogenesisCase-Control StudiesEndothelial CellsFamilial Primary Pulmonary HypertensionFemaleGene Regulatory NetworksHumansLungMaleMiddle AgedPulmonary ArterySignal Transductionendothelial cellspulmonary arterial hypertensionsingle-cell RNA-sequencingsystemic sclerosis

Identifiers

PMID38841857
PMCPMC11269037

What OpenQuestion holds

Textmetadata
LicenceTDM
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.