Evidence map›Paper›PMID 39811555›Full record

ArticleERJ open research2025

Reversal of inflammatory reprogramming by vasodilator agents in pulmonary hypertension.

Anna Kirillova, Meena Sethuraman, Xishuang Dong, Almina Kirdar, Gil Speyer, Yassmin Al Aaraj, Annie Watson, Lily K Schneider, Michael D Creager, Robert Lafyatis and 3 more

Abstract read
In one paragraph

Article in ERJ open research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Anna KirillovaCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Meena SethuramanCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Xishuang DongDepartment of Electrical and Computer Engineering, Center for Computational Systems Biology, Prairie View A&M University, Prairie View, TX, USA.
Almina KirdarCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Gil SpeyerResearch Computing, Arizona State University, Tempe, AZ, USA.
Yassmin Al AarajCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Annie WatsonCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Lily K SchneiderCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Michael D CreagerCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Robert LafyatisDivision of Rheumatology, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA, USA.
Satoshi OkawaCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.
Seungchan KimDepartment of Electrical and Computer Engineering, Center for Computational Systems Biology, Prairie View A&M University, Prairie View, TX, USA.
Stephen Y ChanCenter for Pulmonary Vascular Biology and Medicine, Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Cardiology, Department of Medicine, University of Pittsburgh School of Medicine and UPMC, Pittsburgh, PA, USA.ORCID https://orcid.org/0000-0002-9520-7527

Funding

Defining the Complex Biology of the miR-130/301 Family in Pulmonary HypertensionR01HL124021 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2014 to 2025
$4.9M
Iron-Sulfur Deficiency as a Critical Pathogenic Cause of Pulmonary HypertensionR01HL122596 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHAN, STEPHEN Y · 2015 to 2024
$4.5M
Genetic and hypoxic control of a lncRNA axis orchestrates endothelial reprogramming in pulmonary hypertensionR01HL151228 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Stephen Y Chan · 2023 to 2026
$2.8M
ACTN4 Binding to Functional SNP rs9277336 Controls the Genome Architecture and Endothelial Pathophenotypes in Pulmonary ArterialF30HL170649 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Anna Kirillova · 2023 to 2026
$198k
NHLBI NIH HHS F30 HL170649NHLBI NIH HHS R01 HL122596NHLBI NIH HHS R01 HL124021NHLBI NIH HHS R01 HL151228
6 · The paper itself

Abstract

Background: Pulmonary arterial hypertension (PAH) is a deadly disease without effective non-invasive diagnostic and prognostic testing. It remains unclear whether vasodilators reverse inflammatory activation, a part of PAH pathogenesis. Single-cell profiling of inflammatory cells in blood could clarify these PAH mechanisms. Methods: We evaluated a University of Pittsburgh Medical Center cohort consisting of idiopathic PAH (iPAH) and systemic sclerosis-associated PAH (sscPAH) patients and non-PAH controls. We performed single-cell RNA sequencing of peripheral blood mononuclear cells (PBMCs) from controls (n=3) and from PAH patients (iPAH and sscPAH) naïve to treatment (n=4), PAH patients 3 months after phosphodiesterase-5 inhibitor (PDE5i) treatment (n=7) and PAH patients 3 months after PDE5i+macitentan treatment (n=6). We compared the transcriptomes of five PBMC subtypes from iPAH and sscPAH to observe their serial responses to treatments. Furthermore, we utilised network analysis to illuminate the altered connectivity of biological networks in this complex disease. Results: We defined differential gene expression and perturbed network connectivity in PBMCs of PAH patients following treatment with PDE5i or PDE5i+macitentan. Importantly, we identified significant reversal of inflammatory transcripts and pathways in the combined PAH patient cohort after vasodilator therapy in every PBMC type assessed. The "glucagon signalling in metabolic regulation" pathway in monocytes was reversed after vasodilator therapy Conclusion:

Identifiers

PMID39811555
PMCPMC11726584

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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.