Send to

Choose Destination
Retina. 2014 Dec;34(12):2317-35. doi: 10.1097/IAE.0000000000000349.

Idiopathic epiretinal membrane.

Author information

*Department of Ophthalmology, University Medical Center Groningen, Groningen, the Netherlands; †W. J. Kolff Institute, Graduate School of Medical Sciences, University of Groningen, Groningen, the Netherlands; ‡Tianjin Medical University Eye Hospital, Tianjin Medical University, Tianjin, China; and §Department of Biomedical Engineering, University of Groningen, Groningen, the Netherlands.



Idiopathic epiretinal membrane (iERM) is a fibrocellular membrane that proliferates on the inner surface of the retina at the macular area. Membrane contraction is an important sight-threatening event and is due to fibrotic remodeling.


Analysis of the current literature regarding the epidemiology, clinical features, and pathogenesis of iERM and fibrotic tissue contraction.


Epidemiologic studies report a relationship between iERM prevalence, increasing age, and posterior vitreous detachment. Clinically, iERM progresses through different stages characterized by an increased thickness and wrinkling of the membrane. Pathophysiologically, iERM formation is a fibrotic process in which myofibroblast formation and the deposition of newly formed collagens play key roles. Anomalous posterior vitreous detachment may be a key event initiating the formation of iERM. The age-related accumulation of advanced glycation end products may contribute to anomalous posterior vitreous detachment formation and may also influence the mechanical properties of the iERM.


Remodeling of the extracellular matrix at the vitreoretinal interface by aging and fibrotic changes, plays a significant role in the pathogenesis of iERM. A better understanding of molecular mechanisms underlying this process may eventually lead to the development of effective and nonsurgical approaches to treat and prevent vitreoretinal fibrotic diseases.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Wolters Kluwer
Loading ...
Support Center