Axial elongation of eye

Axial elongation of the eye refers to the increase in the anteroposterior diameter of the eyeball, a central feature in the development and progression of myopia. This elongation is driven by biomechanical remodeling of ocular tissues, with key contributions from the sclera, choroid, and Bruch membrane. It results in stretching and thinning of ocular tissues, increasing risk for complications such as retinal detachment, choroidal and scleral thinning, and visual impairment. The process is regulated by local ocular signaling—especially visual feedback mediated by the retina, as well as genetic and environmental influences. Recent research suggests that scleral endoplasmic reticulum stress, and remodeling of extracellular matrix proteins like collagen, are molecular drivers of this process. Interventions, including pharmacological agents and optical devices, attempt to modulate these pathways to slow progression of myopia by inhibiting further axial elongation. Key clarification: Axial elongation of the eye is not a molecule, protein, receptor, or similar canonical drug target. It is a process, so most of the structured fields are not directly applicable. If a molecular or genetic mediator of axial elongation is the intended target (for example, ATF6 or PERK pathway in the sclera), those can be specified instead for appropriate structured annotation.

Other names

Axial lengthening of eyeEye axial elongationAxial length growth

None specific to this "target" since it is a process, but drugs like atropine may inhibit signaling pathways in the retina or sclera that promote elongation