Frailty and associated factors in women aged 65 years and older with breast cancer: a cross-sectional study.

Epiretinal membrane (ERM) is a proliferation of fibrocellular tissue that forms on the internal surface of the retina and internal limiting membrane (ILM), causing disruption of retinal structure and potentially leading to visual disturbances and metamorphopsia [–]. Prevalence is reported to be between 2.3% and 28.9% in large population studies, with increasing prevalence in older age groups [–]. Idiopathic epiretinal membranes (iERM) form in otherwise healthy eyes, and are most often associated with posterior vitreous detachment []. Micro-damage to the ILM induced by posterior vitreous detachment appears to be the , inducing migration of hyalocytes from the posterior vitreous, retinal pigment epithelium (RPE) cells and activated Muller glial cells from the outer retina to the retinal surface, and subsequent proliferation and fibrocellular differentiation of these cells [–]. In secondary epiretinal membranes (sERM), which may represent 28–32% of all ERMs [, ], the progression of such processes is promoted and amplified by various pre-existing ocular alterations, such as previous ocular surgery, diabetic retinopathy and the presence of peripheral retinal breaks [, –]. Posterior vitreous detachment (PVD) is found less frequently in sERM than in iERM [], suggesting the presence of different mechanisms of activation, migration, and transdifferentiation of resident cells in these membranes, like inflammation and disruption of blood-retinal barrier [, ]. Advanced ERM is characterized by the presence of the ectopic inner foveal layer (EIFL), an abnormal inner retinal tissue caused by traction from the ERM []. Although the exact mechanism of EIFL formation is unclear, sustained anteroposterior and centripetal traction is thought to displace and reorganize the inner retinal layers, forming a continuous layer of inner and middle retinal tissue across the fovea. This traction also activates Müller cells, triggering gliosis and cell proliferation, which are likely involved in the development of EIFL [, ].