Evidence map›Paper›PMID 32553485›Full record

ReviewExperimental eye research2020

Corneal wound healing.

Steven E Wilson

Registry-linked trialAbstract readReview
In one paragraph

Review in Experimental eye research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06854393 (Lacripep, a Novel Investigational Agent, for Corneal Wound Healing and Ocular Surface Homeostasis), which is not on this map. Cited by 139 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
139citing 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.

NCT06854393 phase2recruitingnot on this mapstarted 2025, after this paper: background citation

Lacripep, a Novel Investigational Agent, for Corneal Wound Healing and Ocular Surface Homeostasis

TypeinterventionalSponsorHenry M. Jackson Foundation for the Advancement of Military MedicineRan2025 to 2027Enrolled88ConditionsCorneal Epithelial Wound HealingArms0.00025% Lacripep ophthalmic solution and Placebo
3 · Its place in the literature

Who cites it

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

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
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  8. Review
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  11. Review
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  14. Soluble Epoxide Hydrolase Inhibitors Improve Cornea Alkali Wound Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

79 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

1 author.

Steven E WilsonCole Eye Institute, I-32, Cleveland Clinic, 9500 Euclid Ave, Cleveland, OH, United States. Electronic address: wilsons4@ccf.org.

Funding

Vision Research CoreP30EY001730 · NEI · UNIVERSITY OF WASHINGTON · PI MAUREEN E NEITZ · 1985 to 2026
$23.5M
RESOURCE/SERVICE CORE C - MOLECULAR INFORMATICS MODULEP30EY025585 · NEI · CLEVELAND CLINIC LERNER COM-CWRU · PI Brian D Perkins · 2016 to 2026
$7.7M
Corneal Epithelial Growth Factors and ReceptorsR01EY010056 · NEI · UNIVERSITY OF WASHINGTON · PI WILSON, STEVEN EUGENE · 1994 to 2020
$7.4M
NEI NIH HHS P30 EY001730NEI NIH HHS P30 EY025585NEI NIH HHS R01 EY010056
6 · The paper itself

Abstract

The corneal wound healing response is typically initiated by injuries to the epithelium and/or endothelium that may also involve the stroma. However, it can also be triggered by immune or infectious processes that enter the stroma via the limbal blood vessels. For mild injuries or infections, such as epithelial abrasions or mild controlled microbial infections, limited keratocyte apoptosis occurs and the epithelium or endothelium regenerates, the epithelial basement membrane (EBM) and/or Descemet's basement membrane (DBM) is repaired, and keratocyte- or fibrocyte-derived myofibroblast precursors either undergo apoptosis or revert to the parent cell types. For more severe injuries with extensive damage to EBM and/or DBM, delayed regeneration of the basement membranes leads to ongoing penetration of the pro-fibrotic cytokines transforming growth factor (TGF) β1, TGFβ2 and platelet-derived growth factor (PDGF) that drive the development of mature alpha-smooth muscle actin (SMA)+ myofibroblasts that secrete large amounts of disordered extracellular matrix (ECM) components to produce scarring stromal fibrosis. Fibrosis is dynamic with ongoing mitosis and development of SMA + myofibroblasts and continued autocrine-or paracrine interleukin (IL)-1-mediated apoptosis of myofibroblasts and their precursors. Eventual repair of the EBM and/or DBM can lead to at least partial resolution of scarring fibrosis.

Indexed as

AnimalsApoptosisCorneaCorneal InjuriesExtracellular MatrixHumansMyofibroblastsRegenerationWound HealingCorneaCorneal fibroblastsFibrocytesFibrosisInfectionInjuryInterleukin-1Keratocyte apoptosisMyofibroblastsPDGFScarring. cornealStromal-epithelial interactionsTGF betaWound healing

Identifiers

PMID32553485
PMCPMC7483425

What OpenQuestion holds

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Registered trials

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.