Corneal wound healing

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 a...

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Bibliographic Details
Published in:Experimental eye research Vol. 197; p. 108089
Main Author: Wilson, Steven E.
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01.08.2020
Subjects:
Animals
Apoptosis
Cornea
Cornea - pathology
Corneal fibroblasts
Corneal Injuries - metabolism
Corneal Injuries - pathology
Extracellular Matrix - metabolism
Fibrocytes
Fibrosis
Humans
Infection
Injury
Interleukin-1
Keratocyte apoptosis
Myofibroblasts
Myofibroblasts - pathology
PDGF
Regeneration
Scarring. corneal
Stromal-epithelial interactions
TGF beta
Wound healing
Wound Healing - physiology
Cornea
Interleukin-1
Wound healing
Fibrocytes
Injury
Scarring. corneal
Stromal-epithelial interactions
Infection
PDGF
Fibrosis
Corneal fibroblasts
Keratocyte apoptosis
Myofibroblasts
TGF beta
ISSN:0014-4835, 1096-0007, 1096-0007
Online Access:Get full text
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Summary: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. •Keratocyte apoptosis is the first observable stromal event after anterior corneal injury.•Normal or defective regeneration of the EBM controls regenerative vs. fibrotic healing.•Descemet's membrane modulates regenerative vs. fibrotic healing for posterior injuries.•Fibrosis is dynamic with ongoing mitosis, development and apoptosis of myofibroblasts.
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ISSN:0014-4835
1096-0007
1096-0007
DOI:10.1016/j.exer.2020.108089