Evidence map›Paper›PMID 32640171›Full record

ReviewAmerican journal of respiratory cell and molecular biology2020

You Say You Want a Resolution (of Fibrosis).

Kamran Atabai, Christopher D Yang, Michael J Podolsky

Abstract readReview
In one paragraph

Review in American journal of respiratory cell and molecular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

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

  1. Pooled it
  2. Article
  3. RUNX1 is a mediator of fibrotic activation and epigenetic memory in lung fibroblasts.American journal of respiratory cell and molecular biology · 2026
    Article
  4. Article
  5. Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026
    Review
  6. Article
  7. Pulmonary Fibrosis-Focusing on the Future: Aspen Lung Conference 2024 Summary.American journal of respiratory cell and molecular biology · 2025
    Article
  8. Review
  9. Distinct cAMP Regulation in Scleroderma Lung and Skin Myofibroblasts Governs Their Dedifferentiation via p38α Inhibition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  10. Article
  11. BCL-2 Modulates IRE1α Activation to Attenuate Endoplasmic Reticulum Stress and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2024
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. The M2a Macrophage Phenotype Accompanies Pulmonary Granuloma Resolution inInternational journal of molecular sciences · 2021
    Article
  17. Update in Interstitial Lung Disease 2020.American journal of respiratory and critical care medicine · 2021
    Review
  18. Article
  19. 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

3 authors.

Kamran AtabaiCardiovascular Research Institute.
Christopher D YangCardiovascular Research Institute.ORCID 0000-0002-2090-1880
Michael J PodolskyCardiovascular Research Institute.

Funding

The Role of Collagen Uptake in Regulating the Severity of Pulmonary FibrosisR01HL104009 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ATABAI, KAMRAN · 2011 to 2015
$1.9M
Investigating the role of cell-mediated collagen turnover in regulating tissue fibrosisR01HL136377 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ATABAI, KAMRAN · 2018 to 2021
$1.9M
Role of Endo180 Regulation in Tissue FibrosisK08HL145015 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI PODOLSKY, MICHAEL · 2019 to 2023
$853k
NHLBI NIH HHS K08 HL145015NHLBI NIH HHS R01 HL104009NHLBI NIH HHS R01 HL136377
6 · The paper itself

Abstract

In pathological fibrosis, aberrant tissue remodeling with excess extracellular matrix leads to organ dysfunction and eventual morbidity. Diseases of fibrosis create significant global health and economic burdens and are often deadly. Although fibrosis has traditionally been thought of as an irreversible process, a growing body of evidence demonstrates that organ fibrosis can reverse in certain circumstances, especially if an underlying cause of injury can be removed. This body of evidence has uncovered more and more contributors to persistent and nonresolving tissue fibrosis. Here, we review the present knowledge on resolution of organ fibrosis and restoration of near-normal tissue architecture. We emphasize three critical areas of tissue homeostasis that are necessary for fibrosis resolution, namely, the elimination of matrix-producing cells, the clearance of excess matrix, and the regeneration of normal tissue constituents. In so doing, we also highlight how profibrotic pathways interact with one another and where there may be therapeutic opportunities to intervene and remediate pathological persistent fibrosis.

Indexed as

AnimalsExtracellular MatrixFibroblastsFibrosisHomeostasisHumansMyofibroblastsextracellular matrix turnoverfibroblastsfibrosispulmonary fibrosisresolution of fibrosis

Identifiers

PMID32640171
PMCPMC7528922

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.