Evidence map›Paper›PMID 38791441›Full record

ArticleInternational journal of molecular sciences2024

BMPR2 Loss Activates AKT by Disrupting DLL4/NOTCH1 and PPARγ Signaling in Pulmonary Arterial Hypertension.

Keytam S Awad, Shuibang Wang, Edward J Dougherty, Ali Keshavarz, Cumhur Y Demirkale, Zu Xi Yu, Latonia Miller, Jason M Elinoff, Robert L Danner

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Keytam S AwadCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.ORCID 0000-0002-0165-6939
Shuibang WangCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.
Edward J DoughertyCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.
Ali KeshavarzCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.
Cumhur Y DemirkaleCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.
Zu Xi YuCritical Care Medicine and Pulmonary Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.
Latonia MillerCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.
Jason M ElinoffCritical Care Medicine and Pulmonary Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, MD 20892, USA.ORCID 0000-0002-2376-6370
Robert L DannerCritical Care Medicine Department, Clinical Center, NIH, Bethesda, MD 20892, USA.ORCID 0000-0001-5715-3823

Funding

Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
Cellular Models of PAH-Associated Molecular Defects as a Tool for Identifying New Therapeutic TargetsZIAHL006288 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ELINOFF, JASON · 2023 to 2025
$4.1M
Vascular Dysfunction and InflammationZIACL000188 · CLC · CLINICAL CENTER · PI DANNER, ROBERT L · 2009 to 2025
$0k
NHLBI NIH HHS R24 HL123767
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive cardiopulmonary disease characterized by pathologic vascular remodeling of small pulmonary arteries. Endothelial dysfunction in advanced PAH is associated with proliferation, apoptosis resistance, and endothelial to mesenchymal transition (EndoMT) due to aberrant signaling. DLL4, a cell membrane associated NOTCH ligand, plays a pivotal role maintaining vascular integrity. Inhibition of DLL4 has been associated with the development of pulmonary hypertension, but the mechanism is incompletely understood. Here we report that

Indexed as

Bone Morphogenetic Protein Receptors, Type IIEndothelial CellsPPAR gammaProto-Oncogene Proteins c-aktPulmonary ArteryReceptor, Notch1Signal TransductionAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsCell ProliferationCells, CulturedFemaleHumansHypertension, PulmonaryMalePulmonary Arterial HypertensionAdaptor Proteins, Signal TransducingBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IICalcium-Binding ProteinsDLL4 protein, humanNOTCH1 protein, humanPPAR gammaPPARG protein, humanProto-Oncogene Proteins c-aktReceptor, Notch1AKTBMPR2DLL4endothelial dysfunctionPPARγpulmonary arterial hypertensionsignal transductionvascular remodeling

Identifiers

PMID38791441
PMCPMC11121464

What OpenQuestion holds

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LicenceCC BY
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.