Evidence map›Paper›PMID 31563998›Full record

ReviewCellular and molecular life sciences : CMLS2019

Molecular determinants of mesenchymal cell activation in fibroproliferative diseases.

Loka R Penke, Marc Peters-Golden

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

27 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. 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
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  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Bortezomib Inhibits Lung Fibrosis and Fibroblast Activation without Proteasome Inhibition.American journal of respiratory cell and molecular biology · 2022
    Article
  19. Review
  20. Review
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 1 institution in 1 country.

Loka R PenkeDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, 6301 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109-5642, USA.
Marc Peters-GoldenDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, 6301 MSRB III, 1150 W. Medical Center Drive, Ann Arbor, MI, 48109-5642, USA. petersm@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Novel Functions of Lung Macrophages and Fibroblasts in Pulmonary Inflammation and FibrosisR35HL144979 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2019 to 2025
$6.5M
Control of Fibroblast Function by Prostaglandin E2 and Plasminogen ActivationR01HL094311 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETERS-GOLDEN, MARC L · 2009 to 2017
$3.4M
American Heart Association 15POST25280003NHLBI NIH HHS HL094311NHLBI NIH HHS R01 HL094311NHLBI NIH HHS R35 HL144979
6 · The paper itself

Abstract

Uncontrolled scarring, or fibrosis, can interfere with the normal function of virtually all tissues of the body, ultimately leading to organ failure and death. Fibrotic diseases represent a major cause of death in industrialized countries. Unfortunately, no curative treatments for these conditions are yet available, highlighting the critical need for a better fundamental understanding of molecular mechanisms that may be therapeutically tractable. The ultimate indispensable effector cells responsible for deposition of extracellular matrix proteins that comprise scars are mesenchymal cells, namely fibroblasts and myofibroblasts. In this review, we focus on the biology of these cells and the molecular mechanisms that regulate their pertinent functions. We discuss key pro-fibrotic mediators, signaling pathways, and transcription factors that dictate their activation and persistence. Because of their possible clinical and therapeutic relevance, we also consider potential brakes on mesenchymal cell activation and cellular processes that may facilitate myofibroblast clearance from fibrotic tissue-topics that have in general been understudied.

Indexed as

Cell DifferentiationExtracellular MatrixFibroblastsFibrosisHumansMesenchymal Stem CellsMyofibroblastsRNA, UntranslatedSignal TransductionRNA, UntranslatedApoptosisDe-differentiationDifferentiation proliferationFibroblastFibroproliferative diseasesMyofibroblastSignaling pathways

Identifiers

PMID31563998
PMCPMC6858579
OpenAlexW2975577563

What OpenQuestion holds

Textmetadata
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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.