Abstract
:Myopia is a global problem that is increasing at an epidemic rate in the world. Although the refractive error can be corrected easily, myopes, particularly those with high myopia, are susceptible to potentially blinding eye diseases later in life. Despite a plethora of myopia research, the molecular/cellular mechanisms underlying the development of myopia are not well understood, preventing the search for the most effective pharmacological control. Consequently, several approaches to slowing down myopia progression in the actively growing eyes of children have been underway. So far, atropine, an anticholinergic blocking agent, has been most effective and is used by clinicians in off-label ways for myopia control. Although the exact mechanisms of its action remain elusive and debatable, atropine encompasses a complex interplay with receptors on different ocular tissues at multiple levels and, hence, can be categorized as a shotgun approach to myopia treatment. This review will provide a brief overview of the biological mechanisms implicated in mediating the effects of atropine in myopia control.
Highlights
Myopia is a global problem that is increasing at an epidemic rate in the world
Myopia has been associated with increased risk of comorbidities such as retinal detachment, macular degeneration, foveoschisis, early-onset glaucoma, cataract,[9] and even vision loss,[10] such that the risk is greater at higher degrees of myopia
Despite a plethora of myopia research, the molecular/cellular mechanisms underlying the development of myopia are not well understood, preventing the search for the most effective pharmacological control
Summary
Myopia control using pharmaceutical interventions has been reported to be most effective in comparison with other strategies.[26,27] Anticholinergics are a class of drugs which block the action of acetylcholine at the muscarinic receptors (MRs) on structures with parasympathetic innervation and smooth muscles. Atropine usage is associated with several ocular side-effects such as mydriasis (pupil dilation), photophobia, glare, local allergic response, loss of accommodation, and near vision (cycloplegia), which wear out eventually with the cessation of atropine treatment These side-effects are more common at higher concentrations and seem to be dose-dependent.[31]. In reality, during the washout phase, the change in mean SE and AL elongation was the least (P,0.001) in the 0.01% atropine group,[38] whereas myopia progression continued at a steady pace in groups previously receiving 0.1% and 0.5% atropine, slowing only when 0.01% atropine was restarted in phase 3 This suggests that atropine, at higher concentrations, could induce complex, long-lasting biochemical changes in the mechanisms regulating eye growth. The exact mechanisms mediating atropine action in slowing myopia progression are unclear and remain a matter of speculation
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