Evidence map›Paper›PMID 20363851›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2010

Epithelial repair mechanisms in the lung.

Lynn M Crosby, Christopher M Waters

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 387 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
387citing papers in PubMed, 2 pooled it
47.9field-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

387 citing papers in PubMed, 2 syntheses or guidelines pooled it, 699 citations in OpenAlex.

  1. Pooled it
  2. Association of Matrix Metalloproteinase 9 (Canadian respiratory journal · 2019
    Pooled it
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  13. The importance of mechanical forces in chronic respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
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327 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 1 institution in 1 country.

Lynn M CrosbyDepartments of 1Physiology, University of Tennessee Health Science Center, Memphis, TN 38163-0001, USA.
Christopher M Waters
University of Tennessee Health Science Center · US

Funding

Mechanotransduction in Acute Lung InjuryR01HL094366 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WATERS, CHRISTOPHER M · 2009 to 2012
$2.1M
PHYSIOLOGICAL ADAPTATION TO STRAIN IN AIRWAY EPITHELIUMR01HL064981 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI WATERS, CHRISTOPHER M · 1999 to 2008
$1.9M
Regulation of airway epithelial repairR01HL080417 · NHLBI · UNIVERSITY OF CHICAGO · PI WHITE, STEVEN R · 2006 to 2010
$1.9M
NHLBI NIH HHS HL-064981NHLBI NIH HHS HL-080417NHLBI NIH HHS HL-094366NHLBI NIH HHS R01 HL094366
6 · The paper itself

Abstract

The recovery of an intact epithelium following lung injury is critical for restoration of lung homeostasis. The initial processes following injury include an acute inflammatory response, recruitment of immune cells, and epithelial cell spreading and migration upon an autologously secreted provisional matrix. Injury causes the release of factors that contribute to repair mechanisms including members of the epidermal growth factor and fibroblast growth factor families (TGF-alpha, KGF, HGF), chemokines (MCP-1), interleukins (IL-1beta, IL-2, IL-4, IL-13), and prostaglandins (PGE(2)), for example. These factors coordinate processes involving integrins, matrix materials (fibronectin, collagen, laminin), matrix metalloproteinases (MMP-1, MMP-7, MMP-9), focal adhesions, and cytoskeletal structures to promote cell spreading and migration. Several key signaling pathways are important in regulating these processes, including sonic hedgehog, Rho GTPases, MAP kinase pathways, STAT3, and Wnt. Changes in mechanical forces may also affect these pathways. Both localized and distal progenitor stem cells are recruited into the injured area, and proliferation and phenotypic differentiation of these cells leads to recovery of epithelial function. Persistent injury may contribute to the pathology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis. For example, dysregulated repair processes involving TGF-beta and epithelial-mesenchymal transition may lead to fibrosis. This review focuses on the processes of epithelial restitution, the localization and role of epithelial progenitor stem cells, the initiating factors involved in repair, and the signaling pathways involved in these processes.

Indexed as

Wound HealingAnimalsBlood Coagulation FactorsEicosanoidsEpidermal Growth FactorEpithelial CellsEpitheliumExtracellular Signal-Regulated MAP KinasesFibroblast Growth FactorsHumansInflammation MediatorsIntegrinsInterleukinsLungLung InjuryMatrix MetalloproteinasesBlood Coagulation FactorsEicosanoidsEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesFibroblast Growth FactorsInflammation MediatorsIntegrinsInterleukinsMatrix Metalloproteinases

Identifiers

PMID20363851
PMCPMC2886606
OpenAlexW2130017811

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.