Evidence map›Paper›PMID 37292870›Full record

ArticlemedRxiv : the preprint server for health sciences2023

Lipidomics for diagnosis and prognosis of pulmonary hypertension.

Natalie Bordag, Bence Miklos Nagy, Elmar Zügner, Helga Ludwig, Vasile Foris, Chandran Nagaraj, Valentina Biasin, Ulrich Bodenhofer, Christoph Magnes, Bradley A Maron and 6 more

Open access · greenAbstract readPreprint
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.

  1. Pooled it
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 8 institutions in 4 countries.

Natalie BordagDepartment of Dermatology and Venereology, Medical University of Graz, Graz, Austria.ORCID 0000-0002-9505-6271
Bence Miklos NagyLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0003-3955-4863
Elmar ZügnerInstitute for Biomedical Research and Technologies (HEALTH), Joanneum Research Forschungsgesellschaft m.b.H, Graz, Austria.ORCID 0000-0001-7124-2793
Helga LudwigSchool of Informatics, Communications, and Media, University of Applied Sciences Upper Austria, Hagenberg, Austria.ORCID 0000-0001-6004-1945
Vasile ForisLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0002-8863-0298
Chandran NagarajLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0003-3825-8587
Valentina BiasinLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0002-6277-1463
Ulrich BodenhoferSchool of Informatics, Communications, and Media, University of Applied Sciences Upper Austria, Hagenberg, Austria.ORCID 0000-0001-6859-8828
Christoph MagnesInstitute for Biomedical Research and Technologies (HEALTH), Joanneum Research Forschungsgesellschaft m.b.H, Graz, Austria.ORCID 0000-0002-5153-7444
Bradley A MaronUniversity of Maryland School of Medicine, Baltimore, MD and The University of Maryland-Institute for Health Computing, Bethesda, MD, USA.
Silvia UlrichClinic of Pulmonology, University and University Hospital of Zurich, Zürich, Switzerland.ORCID 0000-0002-5250-5022
Tobias J LangeDepartment of Internal Medicine II, Pulmonology and Critical Care, Kreisklinik Bad Reichenhall, Bad Reichenhall, Germany.
Konrad HötzeneckerDepartment of Thoracic Surgery, Medical University of Vienna, Vienna, Austria.ORCID 0000-0001-6775-7460
Thomas PieberCBmed GmbH, Center for Biomarker Research in Medicine, Graz, Austria.ORCID 0000-0003-3554-0405
Horst OlschewskiLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0002-2834-7466
Andrea OlschewskiLudwig Boltzmann Institute for Lung Vascular Research, Graz, Austria.ORCID 0000-0002-8189-3634
Medical University of Graz · ATJoanneum Research · ATLudwig Boltzmann Institute for Lung Vascular Research · ATUniversity of Applied Sciences Upper Austria · ATKlinik Bad Reichenhall · DEMedical University of Vienna · ATUniversity Hospital of Zurich · CHUniversity of Maryland, Baltimore · US

Funding

Targeting FAK-NEDD9 protein-protein interaction to prevent focal adhesion assembly and vascular proliferation in pulmonary arterial hypertensionR01HL139613 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Sirano Dhe-Paganon, Bradley Maron · 2018 to 2026
$4.1M
Network Medicine and Systems Pharmacology to Advance Precision Medicine in Combined Pulmonary HypertensionR01HL163960 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Evan L Brittain, Anna R Hemnes · 2022 to 2026
$3.4M
NEDD9-SMAD3, fibrinolysis, and chronic thromboembolic pulmonary hypertensionR01HL153502 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI MARON, BRADLEY · 2020 to 2023
$1.7M
Personalized protein-protein interactomes and precision medicine in pulmonary arterial hypertensionR01HL155096 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI MARON, BRADLEY · 2021 to 2024
$1.6M
Austrian Science Fund FWF T 1032NHLBI NIH HHS R01 HL139613NHLBI NIH HHS R01 HL153502NHLBI NIH HHS R01 HL155096NHLBI NIH HHS R01 HL163960
6 · The paper itself

Abstract

Background: Pulmonary hypertension (PH) poses a significant health threat with high morbidity and mortality, necessitating improved diagnostic tools for enhanced management. Current biomarkers for PH lack functionality and comprehensive diagnostic and prognostic capabilities. Therefore, there is a critical need to develop biomarkers that address these gaps in PH diagnostics and prognosis. Methods: To address this need, we employed a comprehensive metabolomics analysis in 233 blood based samples coupled with machine learning analysis. For functional insights, human pulmonary arteries (PA) of idiopathic pulmonary arterial hypertension (PAH) lungs were investigated and the effect of extrinsic FFAs on human PA endothelial and smooth muscle cells was tested Results: PA of idiopathic PAH lungs showed lipid accumulation and altered expression of lipid homeostasis-related genes. In PA smooth muscle cells, extrinsic FFAs caused excessive proliferation and endothelial barrier dysfunction in PA endothelial cells, both hallmarks of PAH.In the training cohort of 74 PH patients, 30 disease controls without PH, and 65 healthy controls, diagnostic and prognostic markers were identified and subsequently validated in an independent cohort. Exploratory analysis showed a highly impacted metabolome in PH patients and machine learning confirmed a high diagnostic potential. Fully explainable specific free fatty acid (FFA)/lipid-ratios were derived, providing exceptional diagnostic accuracy with an area under the curve (AUC) of 0.89 in the training and 0.90 in the validation cohort, outperforming machine learning results. These ratios were also prognostic and complemented established clinical prognostic PAH scores (FPHR4p and COMPERA2.0), significantly increasing their hazard ratios (HR) from 2.5 and 3.4 to 4.2 and 6.1, respectively. Conclusion: In conclusion, our research confirms the significance of lipidomic alterations in PH, introducing innovative diagnostic and prognostic biomarkers. These findings may have the potential to reshape PH management strategies.

Indexed as

biomarkerblood-based testfatty acid to lipid ratiolipidomicsprognosispulmonary hypertension

Identifiers

PMID37292870
PMCPMC10246148
OpenAlexW4377013543

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.