Regulation of Aqueous Humor Outflow
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Glaucoma is the second leading cause of blindness in developed
countries and the leading cause of irreversible blindness worldwide.
The most common form, primary open-angle glaucoma, is often associated
with increased intraocular pressure (IOP) that develops as a result
of increased resistance to outflow of aqueous humor in the conventional
pathway. Today and in the foreseeable future, those with glaucoma
(whether having elevated IOP or not) are managed clinically with
pharmaceutical agents that control IOP. This stems from clinical
trial results showing repeatedly that IOP reduction in open-angle
glaucoma significantly decreases ganglion cell loss over time.
Current therapies lower IOP by targeting aqueous secretion and
uveoscleral outflow, two functions not responsible for elevated
IOP in glaucoma. Unfortunately, the molecular and cellular mechanisms
responsible for changes in conventional outflow function that
result in elevated IOP are currently unknown. Lack of such knowledge
is significant, because understanding the molecular mechanisms
that underlie normal and abnormal regulation of outflow in the
conventional pathway will facilitate the development of more effective
therapies for people with glaucoma. The seminar will present and
discuss current strategies for studying conventional outflow and
for identifying novel drug targets for glaucoma therapy.
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