Evidence map›Paper›PMID 31792399›Full record

ReviewNature reviews. Rheumatology2020

Evasion of apoptosis by myofibroblasts: a hallmark of fibrotic diseases.

Boris Hinz, David Lagares

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 364 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
364citing papers in PubMed, 4 pooled it
37.8field-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

364 citing papers in PubMed, 4 syntheses or guidelines pooled it, 602 citations in OpenAlex.

  1. Pooled it
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  4. Pooled it
  5. Review
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  13. Single-Cell Analysis Reveals the Soft Tissue Structure Heterogeneity Aggravates Peri-Implantitis Through MDK Signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  14. Review
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  19. S100A4 Orchestrates Fibroblast Fate to Drive Fibrotic Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  20. Article

304 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 at 2 institutions in 2 countries.

Boris HinzLaboratory of Tissue Repair and Regeneration, Faculty of Dentistry, University of Toronto, Toronto, Ontario, Canada.ORCID http://orcid.org/0000-0002-0526-393X
David LagaresCenter for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. dlagares@mgh.harvard.edu.ORCID http://orcid.org/0000-0002-7317-8796
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
NHLBI NIH HHS R01 HL147059
6 · The paper itself

Abstract

Organ fibrosis is a lethal outcome of autoimmune rheumatic diseases such as systemic sclerosis. Myofibroblasts are scar-forming cells that are ultimately responsible for the excessive synthesis, deposition and remodelling of extracellular matrix proteins in fibrosis. Advances have been made in our understanding of the mechanisms that keep myofibroblasts in an activated state and control myofibroblast functions. However, the mechanisms that help myofibroblasts to persist in fibrotic tissues remain poorly understood. Myofibroblasts evade apoptosis by activating molecular mechanisms in response to pro-survival biomechanical and growth factor signals from the fibrotic microenvironment, which can ultimately lead to the acquisition of a senescent phenotype. Growing evidence suggests that myofibroblasts and senescent myofibroblasts, rather than being resistant to apoptosis, are actually primed for apoptosis owing to concomitant activation of cell death signalling pathways; these cells are poised to apoptose when survival pathways are inhibited. This knowledge of apoptotic priming has paved the way for new therapies that trigger apoptosis in myofibroblasts by blocking pro-survival mechanisms, target senescent myofibroblast for apoptosis or promote the reprogramming of myofibroblasts into scar-resolving cells. These novel strategies are not only poised to prevent progressive tissue scarring, but also have the potential to reverse established fibrosis and to regenerate chronically injured tissues.

Indexed as

ApoptosisAnimalsExtracellular MatrixFibrosisHumansMyofibroblastsScleroderma, Systemic

Identifiers

PMID31792399
PMCPMC7913072
OpenAlexW2990290007

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.