Evidence map›Paper›PMID 38903104›Full record

ArticlebioRxiv : the preprint server for biology2024

Disruption of DLL4/NOTCH1 Causes Dysregulated PPARγ/AKT 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 readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. 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

5 · Who and what money

Authors and funding

9 authors.

Keytam S AwadCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.ORCID 0000-0002-0165-6939
Shuibang WangCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.
Edward J DoughertyCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.
Ali KeshavarzCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.
Cumhur Y DemirkaleCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.
Zu Xi YuNational Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, US, 20892.
Latonia MillerNational Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, US, 20892.
Jason M ElinoffCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.
Robert L DannerCritical Care Medicine Department, NIH Clinical Center, Bethesda, MD, US, 20892.

Funding

Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
NHLBI NIH HHS R24 HL123767
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a progressive cardiopulmonary disease characterized by 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, activates NOTCH1 signaling and 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

AKTBMPR2DLL4endothelial dysfunctionHPAHIPAHN1ICDPPARγsignal transductionvascular remodeling

Identifiers

PMID38903104
PMCPMC11188078

What Socratic holds

Textmetadata
LicenceCC0
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 Socratic graph.