Cataract remains the leading cause of treatable blindness in the world, are characterized by opacification of the lens, and account for nearly half of all blindness cases[1]. Currently, cataract extraction and intraocular lens (IOL) implantation are the main treatment methods for cataracts. However, surgery of cataract might bring many serious postoperative complications, such as infection, corneal oedema, and high intraocular pressure. Poor postoperative outcomes, cost, and fear of cataract surgery are the most common barriers to cataract surgery [2, 3]. Therefore, it is necessary to elucidate pathogenic mechanisms of cataracts from a new point of view and further provide new targets for effective prevention strategies.
To date, pathogenesis of cataract is not clearly elucidated. A previous study showed that endogenous photosensitive substances in the lens, such as tryptophan and riboflavin, are extremely sensitive to short-wavelength light, which includes UVA and short-wavelength blue light [4].
It is estimated that artificial light sources, including fluorescent light tubes and LEDs, consumed approximately 19% of the electricity produced worldwide in 2012[5]. SWBL mainly comes from artificial light sources. With the widespread use of blue backlight electronic display devices, such as computers and mobile, the human eyes are increasingly exposed to more SWBL[6].
SWBL (400–500 nm), induced oxidative stress and cellular injury, has attracted increasing attention because of the probably injury to the retina [7–9]. The transmission of visible light, especially in the blue spectrum region, is significantly reduced with age. Majority of them is absorbed in lens[10, 11]. It has been suggested a link between exposure to SWBL and the development of cataracts, but additional studies are needed to confirm it.
According to the classification established by the NCCD, cell death is roughly classified as apoptosis, autophagic cell death, necrosis, pyroptosis, etc [12]. In the pathogenesis of cataracts, at least three types of programmed cell death pathways have been studied in deed, including apoptosis[13], autophagy[14], and pyroptosis[15]. The formation of cataracts is not entirely dependent on any single programmed cell death pathway. Of all the types of programmed cell death, apoptosis is the most well understood forms of death. Apoptosis of LECs is a common cellular basis for the formation of cataracts[15]. However, the specific pyroptosis pathway implicated in cataract formation remains to be elucidated.
Pyroptosis and apoptosis depend on particular caspases to motivate their separate programmed cell death pathways. Pyroptosis can be caused by both canonical and noncanonical inflammasome signalling pathways [15–21]. Caspase-1, which leads to the cleavage of GSDMD and induces pore opening on the cytomembrane[22–24], can activate canonical inflammasome signalling pathway.
Our previous animal study indicated that pyroptosis plays a vital role in cataracts formation caused by SWBL exposure. In the present study, SWBL exposure systems were established to discuss the photobiological effects on cultured human LECs, including morphological changes, cell viability and protein levels, as well as the localization of caspase-1 and GSDMD. The results indicated that the caspase-1/GSDMD signalling axis may be involved in the pathological process under SWBL exposure.