Evidence map›Paper›PMID 32437826›Full record

ReviewPharmacology & therapeutics2020

Mechano-therapeutics: Targeting Mechanical Signaling in Fibrosis and Tumor Stroma.

Daniel J Tschumperlin, David Lagares

Abstract readReview
In one paragraph

Review in Pharmacology & therapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
–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

84 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. [Biomechanical properties of epithelial mesenchymal transition in idiopathic pulmonary fibrosis].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2023
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Targeting myeloid cell-mediated fibrosis through FAK.Nature biomedical engineering · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026
    Review
  12. Review
  13. Review
  14. Collagen in Fibrotic Diseases.Sub-cellular biochemistry · 2026
    Review
  15. Review
  16. The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  17. Article
  18. Review
  19. Review
  20. Article

24 more citing papers are in PubMed but not listed here.

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

2 authors.

Daniel J TschumperlinTissue Repair and Mechanobiology Laboratory, Department of Physiology and Biomedical Engineering, Mayo Clinic, 200 1(st) St SW, Rochester, MN 55905, USA. Electronic address: Tschumperlin.daniel@mayo.edu.
David LagaresCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, USA; Department of Medicine, Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Fibrosis Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: dlagares@mgh.harvard.edu.

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
Targeting the ADAM10-sEphrin-B2 pathway in pulmonary fibrosisR01HL147059 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID · 2019 to 2023
$2.1M
NHLBI NIH HHS R01 HL092961NHLBI NIH HHS R01 HL133320NHLBI NIH HHS R01 HL147059
6 · The paper itself

Abstract

Pathological remodeling of the extracellular matrix (ECM) by activated myofibroblasts is a hallmark of fibrotic diseases and desmoplastic tumors. Activation of myofibroblasts occurs in response to fibrogenic tissue injury as well as in tumor-associated fibrotic reactions. The molecular determinants of myofibroblast activation in fibrosis and tumor stroma have traditionally been viewed to include biochemical agents, such as dysregulated growth factor and cytokine signaling, which profoundly alter the biology of fibroblasts, ultimately leading to overexuberant matrix deposition and fibrosis. More recently, compelling evidence has shown that altered mechanical properties of the ECM such as matrix stiffness are major drivers of tissue fibrogenesis by promoting mechano-activation of fibroblasts. In this Review, we discuss new insights into the role of the biophysical microenvironment in the amplified activation of fibrogenic myofibroblasts during the development and progression of fibrotic diseases and desmoplastic tumors. We also summarize novel therapeutic targets for anti-fibrotic therapy based on the mechanobiology of tissue fibrosis and tumor stroma, a class of drugs known as "mechano-therapeutics".

Indexed as

AnimalsBiomechanical PhenomenaCancer-Associated FibroblastsCell Cycle ProteinsExtracellular MatrixFibrosisHumansMyofibroblastsSignal TransductionTranscription FactorsTransforming Growth Factor beta1Cell Cycle ProteinsTranscription FactorsTransforming Growth Factor beta1YY1AP1 protein, humanCAFsFibrosisMechanobiologyMechano-therapeuticsMyofibroblastsTumor Stroma

Identifiers

PMID32437826
PMCPMC7299835

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.