Evidence map›Paper›PMID 34028750›Full record

ReviewMethods in molecular biology (Clifton, N.J.)2021

Animal and Human Models of Tissue Repair and Fibrosis: An Introduction.

David Lagares, Boris Hinz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Methods in molecular biology (Clifton, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
41.6field-weighted citation impact, top 1% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Physical Exercise: A Promising Treatment Against Organ Fibrosis.International journal of molecular sciences · 2025
    Review
  3. Review
  4. Imaging methods to monitor and quantify cell differentiation.Frontiers in cell and developmental biology · 2025
    Review
  5. Review
  6. Article
  7. Article
  8. Getting the Timing Right: Controlling BCL-2 Inhibition as an Antifibrotic Therapy.American journal of respiratory cell and molecular biology · 2024
    Article
  9. Review
  10. The Role of Myofibroblasts in Physiological and Pathological Tissue Repair.Cold Spring Harbor perspectives in biology · 2023
    Review
  11. Review
  12. Article
  13. 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

2 authors at 2 institutions in 2 countries.

David LagaresCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Boris HinzLaboratory of Tissue Repair and Regeneration, Faculty of Dentistry, University of Toronto, Toronto, ON, Canada. boris.hinz@utoronto.ca.
Harvard University · USUniversity of Toronto · CA

Funding

Targeting the ADAM10-sEphrin-B2 pathway in pulmonary fibrosisR01HL147059 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID · 2019 to 2023
$2.1M
CIHR 375597NHLBI NIH HHS R01 HL147059
6 · The paper itself

Abstract

Reductionist cell culture systems are not only convenient but essential to understand molecular mechanisms of myofibroblast activation and action in carefully controlled conditions. However, tissue myofibroblasts do not act in isolation and the complexity of tissue repair and fibrosis in humans cannot be captured even by the most elaborate culture models. Over the past five decades, numerous animal models have been developed to study different aspects of myofibroblast biology and interactions with other cells and extracellular matrix. The underlying principles can be broadly classified into: (1) organ injury by trauma such as prototypical full thickness skin wounds or burns; (2) mechanical challenges, such as pressure overload of the heart by ligature of the aorta or the pulmonary vein; (3) toxic injury, such as administration of bleomycin to lungs and carbon tetrachloride to the liver; (4) organ infection with viruses, bacteria, and parasites, such as nematode infections of liver; (5) cytokine and inflammatory models, including local delivery or viral overexpression of active transforming growth factor beta; (6) "lifestyle" and metabolic models such as high-fat diet; and (7) various genetic models. We will briefly summarize the most widely used mouse models used to study myofibroblasts in tissue repair and fibrosis as well as genetic tools for manipulating myofibroblast repair functions in vivo.

Indexed as

Disease Models, AnimalAnimalsCell Culture TechniquesCell DifferentiationCells, CulturedExtracellular MatrixFibrosisHumansMyofibroblastsWound HealingFibrosisInfectionInflammationInjuryMechanical overloadMouse modelsMyofibroblastToxins

Identifiers

PMID34028750
OpenAlexW3165131946

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.