Background: Glaucoma is an ocular disorder characterized by optic nerve damage which ultimately
causes a progressive and an irreversible loss of vision, often characterized by an elevated intraocular
pressure. Lowering the intraocular pressure (IOP) is the mainstay for glaucoma treatment but
the neuroprotective agents would represent a promising class as the next-generation therapy.
Evidence synthesis: Protein kinases are involved considerably in signal transduction pathways confirmed
by various mechanisms giving the evidence of Rho-kinase to be a versatile therapeutic target. Rho associated protein
kinases also known as ROCK are serine/threonine kinases, belonging to the Ras superfamily of GTPases. The activation
of Rho Kinase results in various actin-myosin arbitrated processes where contraction of actomyosin in the resident
trabecular meshwork (TM) cells and extracellular matrix is responsible for the outflow of aqueous humour. Another major
drawback of the currently available antiglaucoma drugs is their topical use which poses a problem for patient compliance.
The patient intolerability and adherence to the existing therapy therefore call for newer drug delivery systems that would
increase the clinical efficacy of the drugs.
Conclusion: The neuroprotective agents are not considered suitable to be administered through the traditional topical or
oral route. This complementary drug therapy requires a delivery system that could release the drug to the optic nerve in a
sustained manner and also increase patient compliance and tolerability. This review summarizes the use of ROCK inhibitors
that could prevent the damage to the optic nerve along with the reduction in IOP and novel drug delivery systems to
increase the efficacy of the drugs.
Keywords: Glaucoma, Intraocular pressure, Neuroprotective, Rho kinase, Sustained release, Trabecular meshwork.
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