Evidence map›Paper›PMID 32008852›Full record

ReviewTrends in pharmacological sciences2020

Targeting GPCR Signaling for Idiopathic Pulmonary Fibrosis Therapies.

Andrew J Haak, Merrick T Ducharme, Ana M Diaz Espinosa, Daniel J Tschumperlin

Open access · greenAbstract readReview
In one paragraph

Review in Trends in pharmacological sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Systemic sclerosis, main culprits and involved signaling pathways.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  7. Article
  8. Article
  9. Inhibition of AXL ameliorates pulmonary fibrosisThe European respiratory journal · 2025
    Article
  10. Article
  11. Dopamine receptors and organ fibrosis.Biochemistry and biophysics reports · 2025
    Review
  12. Article
  13. Review
  14. Preventive effects of Ramelteon on bleomycin-induced pulmonary fibrosis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Dopamine Receptor D1 Is Exempt from Transforming Growth FactorThe Journal of pharmacology and experimental therapeutics · 2023
    Article
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

4 authors at 1 institution in 1 country.

Andrew J HaakDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA. Electronic address: haak.andrew@mayo.edu.
Merrick T DucharmeDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Ana M Diaz EspinosaDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Daniel J TschumperlinDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, MN, USA.
Mayo Clinic in Florida · US

Funding

Mechanobiology of Lung FibrosisR01HL092961 · NHLBI · MAYO CLINIC ROCHESTER · PI Daniel J. Tschumperlin · 2009 to 2026
$8.0M
Targeting matrix stiffness in lung and liver fibrosisR01HL133320 · NHLBI · MAYO CLINIC ROCHESTER · PI SHAH, VIJAY H., TSCHUMPERLIN, DANIEL J. · 2016 to 2019
$2.2M
NHLBI NIH HHS R01 HL092961NHLBI NIH HHS R01 HL133320
6 · The paper itself

Abstract

A variety of G protein-coupled receptors (GPCRs) have been implicated in the pathogenesis of pulmonary fibrosis, largely through their promotion of profibrotic fibroblast activation. By contrast, recent work has highlighted the beneficial effects of Gαs-coupled GPCRs on reducing fibroblast activation and fibrosis. This review highlights how fibrosis-promoting and -inhibiting GPCR signaling converges on downstream signaling and transcriptional effectors, and how the diversity and dynamics of GPCR expression challenge efforts to identify effective therapies for idiopathic pulmonary fibrosis (IPF). Next-generation strategies to overcome these challenges, focusing on target selection, polypharmacology, and personalized medicine approaches, are discussed as a path towards more effective GPCR-targeted therapies for pulmonary fibrosis.

Indexed as

Idiopathic Pulmonary FibrosisFibrosisHumansPolypharmacologyReceptors, G-Protein-CoupledSignal TransductionReceptors, G-Protein-CoupledfibrosisG protein-coupled receptorMRTFROCKTAZYAP

Identifiers

PMID32008852
PMCPMC7856568
OpenAlexW3003289036

What OpenQuestion holds

Textmetadata
LicenceTDM
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.