Evidence map›Paper›PMID 25830830›Full record

ReviewAnnals of the American Thoracic Society2015

Matrix, mesenchyme, and mechanotransduction.

Daniel J Tschumperlin

Open access · greenAbstract readReview
In one paragraph

Review in Annals of the American Thoracic Society, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.3field-weighted citation impact, top 8% 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, 67 citations in OpenAlex.

  1. Article
  2. Mechanistic basis for the antifibrotic actions of cAMP-based therapies.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  3. The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  4. Loss of lung mesenchymal identities in culture and a screening approach to identify restorative cues.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  5. Article
  6. Local photo-crosslinking of native tissue matrix regulates cell function.bioRxiv : the preprint server for biology · 2024
    Article
  7. Article
  8. Cell-cell interactions and communication dynamics in lung fibrosis.Chinese medical journal pulmonary and critical care medicine · 2024
    Review
  9. Article
  10. Defining the molecular fingerprint of bladder and kidney fibroblasts.American journal of physiology. Renal physiology · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. The life-cycle and restoration of the human vocal fold.Laryngoscope investigative otolaryngology · 2023
    Review
  18. Article
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Daniel J TschumperlinDepartment of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota.
Mayo Clinic · US

Funding

Mechanobiology of Lung FibrosisR01HL092961 · NHLBI · MAYO CLINIC ROCHESTER · PI Daniel J. Tschumperlin · 2009 to 2026
$8.0M
NHLBI NIH HHS HL092961NHLBI NIH HHS R01 HL092961
6 · The paper itself

Abstract

The extracellular matrix (ECM) of the lung serves as both a scaffold for resident cells and a mechanical support for respiratory function. The ECM is deposited during development and undergoes continuous turnover and maintenance during organ growth and homeostasis. Cells of the mesenchyme, including the tissue resident fibroblast, take a leading role in depositing and organizing the matrix and do so in an anatomically distinct fashion, with differing composition, organization, and mechanical properties within the airways, vessels, and alveoli of the lung. Recent technological advancements have allowed the lung's ECM biochemical composition and mechanical properties to be studied with improved resolution, thereby identifying novel disease-related changes in ECM characteristics. In parallel, efforts to study cells seeded on normal and disease-derived matrices have illustrated the powerful role the ECM can play in altering key functions of lung resident cells. The mechanical properties of the matrix have been identified as an important modifier of cell-matrix adhesions, with matrices of pathologic stiffness promoting profibrotic signaling and cell function. Ongoing work is identifying both mechanically activated pathways in mesenchymal cells and disease-related ECM molecules that biochemically regulate cell function. Uncovering the control systems by which cells respond to and regulate the matrix, and the failures in these systems that underlie aberrant repair, remains a major challenge. Progress in this area will be an essential element in efforts to engineer functional lung tissue for regenerative approaches and will be key to identifying new therapeutic strategies for lung diseases characterized by disturbed matrix architecture.

Indexed as

Extracellular MatrixFibroblastsHumansMechanotransduction, CellularMesodermPulmonary Fibrosisextracellular matrixfibroblastfibrosislung

Identifiers

PMID25830830
PMCPMC4430972
OpenAlexW1970854145

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.