Lens Cytoskeleton: An Update on the Etiopathogenesis of Human Cataracts

Abstract

A cataract is a loss of the transparency of a normal crystalline lens. Multiple factors, including age as the major risk factor for cataracts, can disturb the transparency of the crystalline lens due to cumulative damage from environmental insults to proteins, particularly crystallins. Lens proteins do not turnover, and crystallins undergo extensive post-translational modifications (PTMs) with age in order to interact with each other and maintain their soluble basis for lens transparency. These PTMs include truncation, oxidation, deamidation, acetylation, phosphorylation, and glycosylation. Cataract formation, apart from protein PTMs, involves protein crosslinking, protein insolubilization, and aggregation. Oxidation is a key feature in age-related cataract formation. Due to the role of genetic and environmental factors, as well as its variable clinical presentation, we consider cataracts to be a multifactorial disease. The preliminary results of our study indicate that proteins implicated in the pathway of a structural constituent of the eye lens (BFSP1, BFSP2, CRYAA, CRYAB, CRYBA, CRYBB, CRYGC, CRYGD, CRYGS, KRTs, and VIM), together with AQP1 and AQP5, may also be involved in lens aging.