Abstract
Conjunctival and subconjunctival fibrogenesis and inflammation are sight compromising side effects that can occur subsequent to glaucoma filtration surgery. Despite initial declines in intraocular pressure resulting from increasing aqueous outflow, one of the activated responses includes marshalling of proinflammatory and pro-fibrogenic cytokine mediator entrance into the aqueous through a sclerostomy window and their release by local cells, as well as infiltrating activated immune cells. These changes induce dysregulated inflammation, edema and extracellular matrix remodeling, which occlude outflow facility. A number of therapeutic approaches are being taken to offset declines in outflow facility since the current procedure of inhibiting fibrosis with either mitomycin C (MMC) or 5-fluorouracil (5-FU) injection is nonselective. One of them entails developing a new strategy for reducing fibrosis induced by wound healing responses including myofibroblast transdifferentiation and extracellular matrix remodeling in tissue surrounding surgically created shunts. The success of this endeavor is predicated on having a good understanding of conjunctival wound healing pathobiology. In this review, we discuss the roles of inappropriately activated growth factor and cytokine receptor linked signaling cascades inducing conjunctival fibrosis/scarring during post-glaucoma surgery wound healing. Such insight may identify drug targets for blocking fibrogenic signaling and excessive fibrosis which reduces rises in outflow facility resulting from glaucoma filtration surgery.
Highlights
It is estimated in 2010 that there were more than 60.5 million people worldwide with glaucoma and this number is expected to increase to reach 79.6 million by 2020 [1]
Roles of aqueous humor-derived growth factors/cytokines on conjunctival bleb scarring Variations in the aqueous humor TGF-β2 ratio between its active and inactive forms are postulated to modulate the filtering bleb, and fibrotic reactions induced by local fibroblasts [15], Increases in the ratio of this growth factor occurs in tissues compromised by injury
Roles of growth factors/cytokines expressed in local fibroblasts and inflammatory cells on conjunctival bleb scarring Besides increasing aqueous humor growth factor and cytokine levels, injury toconjunctival tissue resulting from surgical intervention activates local tissue cells, e.g., fibroblasts and induces proinflammatory neutrophils and macrophages infiltration into a wound
Summary
It is estimated in 2010 that there were more than 60.5 million people worldwide with glaucoma and this number is expected to increase to reach 79.6 million by 2020 [1]. Tissue fibrosis resulting from an overly driven wound healing response may impair filtering bleb formation and reduce aqueous humor outflow causing reversal of the initial decline in intraocular pressure. We deal here with the pathobiological subconjunctival wound healing responses induced by glaucoma filtration surgery, which affect the duration of the pressure lowering effect of this procedure.
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