Sulforaphane promotes ER stress, autophagy, and cell death: implications for cataract surgery

Cataract renders millions of people blind throughout the world. Despite recent advances in putative cataract treatments, the only currently accepted means of resolving the problem is through surgical intervention [ 1 , 2 ]. Cataract removal is the most common surgical procedure in the world and is a huge drain on healthcare providers [ 3 , 4 ]. Posterior capsule opacification (PCO) is the most common complication of cataract surgery and likely the most common cause of nonrefractive decreased postoperative vision [ 5 , 6 ]. PCO occurs in a significant proportion of cataract surgery patients within 5 years postoperatively, depending on age, geographic location, and the type of intraocular lens (IOL) placed during cataract surgery [ 2 , 7 ]. PCO reflects the wound-healing process of the lens epithelial cells (LECs) that remain in the capsular bag after cataract surgery. Residual LECs within the capsular bag rapidly grow and proliferate across the posterior lens capsule, which can encroach upon the visual axis and cause a secondary reduction in vision quality [ 8 ]. Treatment of PCO is usually straightforward and effective, using the neodymium:YAG (Nd:YAG) laser to cut an opening in the posterior lens capsule, thus clearing the visual axis and restoring vision [ 2 ]. However, disruption of the posterior capsule due to complications of cataract surgery results in a relative increase in the occurrence of complications such as an elevation in intraocular pressure, retinal cystoid macular edema, glaucoma, intraocular lens damage, iritis, endophthalmitis, and retinal detachment [ 9 ]. Nd:YAG treatment is the second most common corrective surgery, which provides further cost to healthcare providers not to mention the reduced quality of life experienced by the patient as PCO develops. Thus, PCO is an important problem, and thus, improved management of this condition is required. A number of strategies have been proposed but are yet to reach the clinic. These include mechanical approaches, which strive to remove all LECs during surgery or by altering shape and materials of the IOL designs [ 10 , 11 ]. Different pharmaceutical methods to prevent PCO by removing or destroying residual LECs have also been proposed that can either arrest growth, prevent matrix contraction, or destroy the entire lens cell population [ 12 – 15 ].