The oxidative stress regulatory mechanism of autophagy and apoptosis in lens epithelial cells.

Cataract is the leading cause of blindness worldwide, and its incidence rate is still on the rise. Oxidative stress plays a key role in the formation of cataracts. Oxidative stress not only causes damage to lens epithelial cells (LECs) but also activates autophagy and apoptosis. Specifically, under oxidative stress conditions, the apoptosis of LECs is significantly activated, which in turn leads to accelerated lens opacity and cataract development. Meanwhile, autophagy, as a cellular self-protection mechanism, exhibits bidirectional regulatory characteristics in response to oxidative stress. In addition, in diabetic cataracts, high glucose levels can disrupt the balance between autophagy and oxidative stress, exacerbating LECs damage. This cross-effect of apoptosis and autophagy highlights the core position of both in the pathogenesis of cataracts, but the specific molecular mechanism still needs to be further clarified. Although antioxidants can alleviate apoptosis and autophagy damage induced by oxidative stress, the clinical treatment of cataracts still urgently needs prevention and treatment strategies targeting molecular mechanisms.