Evidence map›Paper›PMID 32058955›Full record

ArticleiScience2020

Principles of Cell Circuits for Tissue Repair and Fibrosis.

Miri Adler, Avi Mayo, Xu Zhou, Ruth A Franklin, Matthew L Meizlish, Ruslan Medzhitov, Stefan M Kallenberger, Uri Alon

Abstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed, 2 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

89 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
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  7. Review
  8. Article
  9. Article
  10. Article
  11. Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
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29 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

8 authors.

Miri AdlerDepartment Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel; Broad Institute of Massachusetts Institute of Technology and Harvard, Cambridge, MA 02142, USA.
Avi MayoDepartment Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.
Xu ZhouHoward Hughes Medical Institute Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Ruth A FranklinHoward Hughes Medical Institute Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Matthew L MeizlishHoward Hughes Medical Institute Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Ruslan MedzhitovHoward Hughes Medical Institute Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06510, USA.
Stefan M KallenbergerDigital Health Center, Berlin Institute of Health (BIH) and Charité, Berlin 10178, Germany; Division of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany.
Uri AlonDepartment Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel. Electronic address: uri.alon@weizmann.ac.il.

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007205 · NIGMS · YALE UNIVERSITY · PI KAZMIERCZAK, BARBARA I · 1985 to 2019
$42.9M
Role of GDF15 in the Regulation of Host Tolerance to InflammationR01AI144152 · NIAID · YALE UNIVERSITY · PI MEDZHITOV, RUSLAN · 2019 to 2023
$2.1M
Macrophage regulation of tissue repair and fibrosis through sensing of extracellular matrix mechanicsF31HL139116 · NHLBI · YALE UNIVERSITY · PI MEIZLISH, MATTHEW LOWELL · 2018 to 2019
$59k
Cancer Research UK 27145NHLBI NIH HHS F31 HL139116NIAID NIH HHS R01 AI144152NIGMS NIH HHS T32 GM007205
6 · The paper itself

Abstract

Tissue repair is a protective response after injury, but repetitive or prolonged injury can lead to fibrosis, a pathological state of excessive scarring. To pinpoint the dynamic mechanisms underlying fibrosis, it is important to understand the principles of the cell circuits that carry out tissue repair. In this study, we establish a cell-circuit framework for the myofibroblast-macrophage circuit in wound healing, including the accumulation of scar-forming extracellular matrix. We find that fibrosis results from multistability between three outcomes, which we term "hot fibrosis" characterized by many macrophages, "cold fibrosis" lacking macrophages, and normal wound healing. This framework clarifies several unexplained phenomena including the paradoxical effect of macrophage depletion, the limited time-window in which removing inflammation leads to healing, and why scar maturation takes months. We define key parameters that control the transition from healing to fibrosis, which may serve as potential targets for therapeutic reduction of fibrosis.

Indexed as

In Silico BiologySystems BiologyTissue Engineering

Identifiers

PMID32058955
PMCPMC7005469

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.