Evidence map›Paper›PMID 37628831›Full record

ReviewInternational journal of molecular sciences2023

Pharmacology and Rationale for Seralutinib in the Treatment of Pulmonary Arterial Hypertension.

Soni Savai Pullamsetti, Ravikumar Sitapara, Robin Osterhout, Astrid Weiss, Laura L Carter, Lawrence S Zisman, Ralph Theo Schermuly

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
5.4field-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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. CSF-1 receptor blockade in pulmonary arterial hypertension-keeping macrophages in check?American journal of respiratory cell and molecular biology · 2026
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Pathophysiology and Treatment of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024
    Article
  12. Review
4 · The record

Corrections and comments

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

7 authors at 2 institutions in 2 countries.

Soni Savai PullamsettiLung Vascular Epigenetics, Center for Infection and Genomics of the Lung (CIGL), Justus-Liebig-Universität Gießen, Aulweg 132, 35392 Giessen, Germany.ORCID 0000-0003-0440-8831
Ravikumar SitaparaGossamer Bio, Inc., San Diego, CA 92121, USA.
Robin OsterhoutGossamer Bio, Inc., San Diego, CA 92121, USA.ORCID 0000-0003-1146-9915
Astrid WeissUGMLC Pulmonale Pharmakotherapie, Biomedizinisches Forschungszentrum Seltersberg (BFS), Justus-Liebig-Universität Gießen, Schubertstraße 81, 35392 Giessen, Germany.
Laura L CarterGossamer Bio, Inc., San Diego, CA 92121, USA.
Lawrence S ZismanGossamer Bio, Inc., San Diego, CA 92121, USA.
Ralph Theo SchermulyDepartment of Internal Medicine, Justus-Liebig-University Giessen, Aulweg 130, 35392 Giessen, Germany.ORCID 0000-0002-5167-6970
Gossamer Bio (United States) · USJustus-Liebig-Universität Gießen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a complex disorder characterized by vascular remodeling and a consequent increase in pulmonary vascular resistance. The histologic hallmarks of PAH include plexiform and neointimal lesions of the pulmonary arterioles, which are composed of dysregulated, apoptosis-resistant endothelial cells and myofibroblasts. Platelet-derived growth factor receptors (PDGFR) α and β, colony stimulating factor 1 receptor (CSF1R), and mast/stem cell growth factor receptor kit (c-KIT) are closely related kinases that have been implicated in PAH progression. In addition, emerging data indicate significant crosstalk between PDGF signaling and the bone morphogenetic protein receptor type 2 (BMPR2)/transforming growth factor β (TGFβ) receptor axis. This review will discuss the importance of the PDGFR-CSF1R-c-KIT signaling network in PAH pathogenesis, present evidence that the inhibition of all three nodes in this kinase network is a potential therapeutic approach for PAH, and highlight the therapeutic potential of seralutinib, currently in development for PAH, which targets these pathways.

Indexed as

Pulmonary Arterial HypertensionEndothelial CellsFamilial Primary Pulmonary HypertensionHumansProtein Kinase InhibitorsProto-Oncogene Proteins c-kitReceptor Protein-Tyrosine KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-kitReceptor Protein-Tyrosine KinasesABLc-KITCSF1RdasatinibimatinibinhalationPDGFR

Identifiers

PMID37628831
PMCPMC10454154
OpenAlexW4385740554

What Socratic holds

Textmetadata
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 Socratic graph.