Evidence map›Paper›PMID 29293088›Full record

ReviewThe Journal of clinical investigation2018

Extracellular matrix as a driver of progressive fibrosis.

Jeremy Herrera, Craig A Henke, Peter B Bitterman

Abstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 374 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
374citing 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

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

  1. Pooled it
  2. Potential role of CTHRC1 in renal fibrosis.Molecular biology reports · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Hepatic stellate cells in alcoholic liver cirrhosis: mechanisms of fibrogenesis, plasticity, and fibrosis reversal.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  11. Article
  12. Review
  13. Review
  14. RUNX1 is a mediator of fibrotic activation and epigenetic memory in lung fibroblasts.American journal of respiratory cell and molecular biology · 2026
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

314 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

3 authors.

Jeremy Herrera
Craig A Henke
Peter B Bitterman

Funding

TRAINING-PULMONARY CELL &MOLECULAR BIOLOGY &PHYSIOLOGYT32HL007741 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DUDLEY, R. ADAMS, INGBAR, DAVID H · 1994 to 2023
$13.9M
Role of fibrotic extracellular matrix in generating the IPF FibroblastR01HL125236 · NHLBI · UNIVERSITY OF MINNESOTA · PI BITTERMAN, PETER B · 2015 to 2018
$1.9M
Integrin-Matrix Regulation of IPF Fibroblast PhenotypeR01HL125227 · NHLBI · UNIVERSITY OF MINNESOTA · PI HENKE, CRAIG A · 2015 to 2018
$1.8M
NHLBI NIH HHS R01 HL125227NHLBI NIH HHS R01 HL125236NHLBI NIH HHS T32 HL007741
6 · The paper itself

Abstract

The extracellular matrix (ECM) is dynamically tuned to optimize physiological function. Its major properties, including composition and mechanics, profoundly influence cell biology. Cell-ECM interactions operate through an integrated set of sensor and effector circuits that use several classes of receptors and signal transduction pathways. At the single-cell level, the ECM governs differentiation, metabolism, motility, orientation, proliferation, and survival. At the cell population level, the ECM provides higher-order guidance that is essential for physiological function. When pathological changes in the ECM lead to impairment of organ function, we use the term "fibrosis." In this Review, we differentiate fibrosis initiation from progression and focus primarily on progressive lung fibrosis impairing organ function. We present a working model to explain how the altered ECM is not only a consequence but also a driver of fibrosis. Additionally, we advance the concept that fibrosis progression occurs in a fibrogenic niche that is composed of a fibrogenic ECM that nurtures fibrogenic mesenchymal progenitor cells and their fibrogenic progeny.

Indexed as

Cell MovementCell PolaritySignal TransductionAnimalsCell DifferentiationExtracellular MatrixFibrosisHumansLung DiseasesMesenchymal Stem Cells

Identifiers

PMID29293088
PMCPMC5749528

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.