Regulation of scleral metabolism in myopia and the role of transforming growth factor-beta

Myopia is one of the most prevalent ocular conditions and is the result of a mismatch between the power of the eye and axial length of the eye. In the vast majority of cases the structural cause of myopia is an excessive axial length of the eye, or more specifically the vitreous chamber depth. In about 3% of the general population in Europe, USA and Australia, the degree of myopia is above 6 dioptres and is termed high myopia. In South East Asia the figure is closer to 20% of the general population with high myopia. The prevalence of sight threatening ocular pathology is markedly increased in eyes with high degrees of myopia (>−6 D). This results from the excessive axial elongation of the eye which, by necessity, must involve the outer coat of the eye, the sclera. Current theories of refractive development acknowledge the pivotal role of the sclera in the control of eye size and the development of myopia. This review details the major structural, biochemical and biomechanical changes that underlie abnormal development of the mammalian sclera in myopia. In describing the changes in regulation of sclera metabolism in myopia, the pivotal role of transforming growth factor-β signalling is highlighted as the responsible factor for certain critical events in myopia development that ultimately result in the scleral pathology observed in high myopia.

► The sclera undergoes marked changes in structure, biochemistry and biomechanical properties in myopia. ► Reductions in scleral collagen & glycosaminoglycan synthesis and TGF-β isoforms in myopia. ► There are changes in collagen degradation and creep properties in the sclera of myopic eyes. ► TGF-β is the central mediator of the changes in the sclera of myopic eyes.