Evidence map›Paper›PMID 33052714›Full record

ArticleAmerican journal of respiratory cell and molecular biology2021

Targeting Jak-Stat Signaling in Experimental Pulmonary Hypertension.

Dinesh Yerabolu, Astrid Weiss, Baktybek Kojonazarov, Mario Boehm, Beate Christiane Schlueter, Clemens Ruppert, Andreas Günther, Danny Jonigk, Friedrich Grimminger, Hossein-Ardeschir Ghofrani and 3 more

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In one paragraph

Article in American journal of respiratory cell and molecular biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 4% of its field
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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
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  4. Journal of thoracic disease · 2026
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  11. Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 2 institutions in 1 country.

Dinesh YeraboluJustus-Liebig-University Giessen, Giessen, Germany.
Astrid WeissJustus-Liebig-University Giessen, Giessen, Germany.
Baktybek KojonazarovJustus-Liebig-University Giessen, Giessen, Germany.
Mario BoehmJustus-Liebig-University Giessen, Giessen, Germany.
Beate Christiane SchlueterJustus-Liebig-University Giessen, Giessen, Germany.
Clemens RuppertJustus-Liebig-University Giessen, Giessen, Germany.
Andreas GüntherJustus-Liebig-University Giessen, Giessen, Germany.
Danny JonigkGerman Center for Lung Research, Giessen, Germany.
Friedrich GrimmingerJustus-Liebig-University Giessen, Giessen, Germany.
Hossein-Ardeschir GhofraniJustus-Liebig-University Giessen, Giessen, Germany.
Werner SeegerJustus-Liebig-University Giessen, Giessen, Germany.
Norbert WeissmannJustus-Liebig-University Giessen, Giessen, Germany.
Ralph Theo SchermulyJustus-Liebig-University Giessen, Giessen, Germany.
Justus-Liebig-Universität Gießen · DEMedizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In pulmonary arterial hypertension (PAH), progressive structural remodeling accounts for the pulmonary vasculopathy including the obliteration of the lung vasculature that causes an increase in vascular resistance and mean blood pressure in the pulmonary arteries ultimately leading to right heart failure-mediated death. Deciphering the molecular details of aberrant signaling of pulmonary vascular cells in PAH is fundamental for the development of new therapeutic strategies. We aimed to identify kinases as new potential drug targets that are dysregulated in PAH by means of a peptide-based kinase activity assay. We performed a tyrosine kinase-dependent phosphorylation assay using 144 selected microarrayed substrate peptides. The differential signature of phosphopeptides was used to predict alterations in tyrosine kinase activities in human pulmonary arterial smooth muscle cells (HPASMCs) from patients with idiopathic PAH (IPAH) compared with healthy control cells. Thereby, we observed an overactivation and an increased expression of Jak2 (Janus kinase 2) in HPASMCs from patients with IPAH as compared with controls.

Indexed as

AnimalsCells, CulturedHumansHypertension, PulmonaryHypertrophy, Right VentricularJanus KinasesMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleNitrilesPulmonary ArteryPyrazolesPyrimidinesRatsJanus KinasesNitrilesPyrazolesPyrimidinesruxolitinibSTAT Transcription Factorsexperimental pulmonary hypertensionJak–Stat signalingkinase inhibitorspeptide-based kinase activity assayruxolitinib

Identifiers

PMID33052714
OpenAlexW3093166712

What OpenQuestion holds

Textmetadata
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.