Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing 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.
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
12 authors.
Maki Niihori *Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0002-3013-7628
Joel James *Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0001-9458-5457
Mathews V VargheseDivision of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0002-8552-7359
Nolan McClainDepartment of Medicine, University of Arizona, Tucson, AZ, USA.ORCID 0009-0003-7576-0477
Odunayo Susan LawalDivision of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0003-4365-7427
Rohit C PhilipDepartment of Electrical and Computer Engineering, University of Arizona College of Engineering, Tucson, AZ, USA.ORCID 0009-0008-2402-5196
Brenda K BaggettThe University of Arizona Cancer Center, University of Arizona , Tucson, AZ, USA.ORCID 0009-0006-7073-6795
Dmitry A GoncharovDivision of Pulmonary, Critical Care and Sleep Medicine, Lung Center, University of California, Davis School of Medicine, Davis, CA, USA.ORCID 0000-0002-8286-785X
Vinicio de Jesus PerezDivision of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, CA, USA.ORCID 0000-0001-5532-8247
Elena A GoncharovaDivision of Pulmonary, Critical Care and Sleep Medicine, Lung Center, University of California, Davis School of Medicine, Davis, CA, USA.ORCID 0000-0001-7118-6752
Ruslan RafikovDivision of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0001-5950-4076
Olga RafikovaDivision of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, IN, USA.ORCID 0000-0002-4517-7075
Funding
Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
The Wnt7a/ROR2 axis in the pathogenesis of pulmonary arterial hypertensionR01HL134776 · NHLBI · STANFORD UNIVERSITY · PI DE JESUS PEREZ, VINICIO A · 2017 to 2025
$5.0M
Endothelial-pericyte interactions in the pathogenesis of pulmonary arterial hypertensionR01HL139664 · NHLBI · STANFORD UNIVERSITY · PI DE JESUS PEREZ, VINICIO A · 2018 to 2025
$4.7M
Anaplerotic reprogramming of endothelial cells in pulmonary hypertension.R01HL132918 · NHLBI · UNIVERSITY OF ARIZONA · PI RAFIKOV, RUSLAN · 2016 to 2025
$4.5M
Hemolysis and Free Heme Signaling in Pulmonary HypertensionR01HL151447 · NHLBI · UNIVERSITY OF ARIZONA · PI Ruslan Rafikov · 2020 to 2026
$4.3M
HIPPO Signaling in Pulmonary Arterial HypertensionR01HL130261 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GONCHAROVA, ELENA · 2016 to 2023
$3.5M
Mitochondrial Dysfunction in Pulmonary HypertensionR01HL160666 · NHLBI · UNIVERSITY OF ARIZONA · PI Olga Rafikova · 2022 to 2026
$3.3M
Pericytes and postnatal alveolarization: Role of hypoxia inducible factorsR01HL160018 · NHLBI · STANFORD UNIVERSITY · PI ALVIRA, CRISTINA MARIA, CORNFIELD, DAVID N. · 2022 to 2025
$2.6M
GATA-6 in pulmonary arterial hypertensionR01HL150638 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI GONCHAROVA, ELENA, TROJANOWSKA, MARIA · 2020 to 2023
$2.6M
LDHA-lactate signaling in pulmonary arterial hypertensionR01HL172488 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Elena Goncharova · 2024 to 2026
$2.0M
HMGBG1 and Gender Difference in Pulmonary Arterial HypertensionR01HL133085 · NHLBI · UNIVERSITY OF ARIZONA · PI RAFIKOVA, OLGA · 2016 to 2020
$1.9M
Aminopeptidase N Driven Signaling in the Development of Pulmonary HypertensionR00HL171869 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI Joel James · 2025 to 2026
Impaired pulmonary angiogenesis plays a pivotal role in the progression of pulmonary arterial hypertension (PAH) and patient mortality, yet the molecular mechanisms driving this process remain enigmatic. Our study uncovered a striking connection between mitochondrial dysfunction (MD), caused by a humanized mutation in the NFU1 gene, and severely disrupted pulmonary angiogenesis in adult lungs. Restoring the bioavailability of the NFU1 downstream target, lipoic acid (LA), alleviated MD and angiogenic deficiency and rescued the progressive PAH phenotype in the NFU1G206C model. Notably, significant NFU1 expression and signaling insufficiencies were also identified in idiopathic PAH (iPAH) patients' lungs, emphasizing this study's relevance beyond NFU1 mutation cases. The remarkable improvement in mitochondrial function of PAH patient-derived pulmonary artery endothelial cells (PAECs) following LA supplementation introduces LA as a potential therapeutic approach. In conclusion, this study unveils a novel role for MD in dysregulated pulmonary angiogenesis and PAH manifestation, emphasizing the need to correct MD in PAH patients with unrecognized NFU1/LA deficiency.
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.
Mitochondria as a primary determinant of angiogenic modality in pulmonary arterial hypertension. · full record | OpenQuestion