PURPOSE: To provide an overview of the importance of the coordinated role of the epithelial basement membrane (EBM) and Descemet's basement membrane (DBM) in modulating scarring (fibrosis) in the cornea after injuries, infections, surgeries, and diseases of the cornea. METHODS: Literature review. RESULTS: Despite their molecular and ultrastructural differences, the EBM and DBM act in a coordinated fashion to modulate the entry of transforming growth factor beta (TGF-β) and other growth factors from the epithelium/tear film and aqueous humor, respectively, into the corneal stroma where persistent levels of these modulators trigger the development and persistence of myofibroblasts that produced disordered, opaque extracellular matrix not usually present in the corneal stroma. The development of these myofibroblasts and the extracellular matrix they produce is often detrimental to visual function of the cornea after penetrating keratoplasty, LASIK buttonhole flaps, persistent epithelial defects, microbial keratitis, Descemet stripping automated endothelial keratoplasty, or Descemet membrane endothelial keratoplasty, while being beneficial in other situations such as the scarred edge of LASIK flaps and donor-recipient interface in penetrating keratoplasty. Efforts to modulate the repair or replacement of the EBM and DBM, and thereby the development or disappearance of myofibroblasts, should be a major emphasis of treatments provided by refractive and corneal surgeries, infections, trauma, or diseases of the cornea. CONCLUSIONS: The EBM and DBM are critical modulators of the localization of profibrotic growth factors, such as TGF-β, that modulate the development and persistence of myofibroblasts that produce corneal scars (stromal fibrosis). Therapeutic efforts to regenerate or repair EBM and/or DBM, and interfere with the development of myofibroblasts or facilitate their disappearance are often the key to clinical outcomes. [J Refract Surg. 2019;35(8):506-516.]. Copyright 2019, SLACK Incorporated.
PURPOSE: To provide an overview of the importance of the coordinated role of the epithelial basement membrane (EBM) and Descemet's basement membrane (DBM) in modulating scarring (fibrosis) in the cornea after injuries, infections, surgeries, and diseases of the cornea. METHODS: Literature review. RESULTS: Despite their molecular and ultrastructural differences, the EBM and DBM act in a coordinated fashion to modulate the entry of transforming growth factor beta (TGF-β) and other growth factors from the epithelium/tear film and aqueous humor, respectively, into the corneal stroma where persistent levels of these modulators trigger the development and persistence of myofibroblasts that produced disordered, opaque extracellular matrix not usually present in the corneal stroma. The development of these myofibroblasts and the extracellular matrix they produce is often detrimental to visual function of the cornea after penetrating keratoplasty, LASIK buttonhole flaps, persistent epithelial defects, microbial keratitis, Descemet stripping automated endothelial keratoplasty, or Descemet membrane endothelial keratoplasty, while being beneficial in other situations such as the scarred edge of LASIK flaps and donor-recipient interface in penetrating keratoplasty. Efforts to modulate the repair or replacement of the EBM and DBM, and thereby the development or disappearance of myofibroblasts, should be a major emphasis of treatments provided by refractive and corneal surgeries, infections, trauma, or diseases of the cornea. CONCLUSIONS: The EBM and DBM are critical modulators of the localization of profibrotic growth factors, such as TGF-β, that modulate the development and persistence of myofibroblasts that produce corneal scars (stromal fibrosis). Therapeutic efforts to regenerate or repair EBM and/or DBM, and interfere with the development of myofibroblasts or facilitate their disappearance are often the key to clinical outcomes. [J Refract Surg. 2019;35(8):506-516.]. Copyright 2019, SLACK Incorporated.
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