Role of crystallins in ocular neuroprotection and axonal regeneration.

摘要: Neuroprotection is an emerging challenge in ophthalmology due to the particularly exposed location of retinal neurons and steadily increasing rate intraocular surgical pharmacological treatments applied various eye diseases. Within few decades neuroprotection has developed from strongly contested approaches being recognized introduced as a potentially clinical application. One groups putative substances for comprises αA- αB-crystallins, which are types heat-shock proteins considered be molecular chaperones. The β/γ-crystallins form their own superfamily characterized with distinct structure containing four Greek key motifs. Besides abundant ocular lens, crystallins also expressed both developing mature retina. Crystallins dramatically up-regulated numerous pathologies, including mechanical injury, ischemic insults, age-related macular degeneration, uveoretinitis, diabetic retinopathy. α family thought play crucial role neuron survival inflammation. β/γ small possible tissue remodeling repair. typical diseases associated experimental glaucomatous neuropathy that by expression. Another disease atrophy occurs after injury optic nerve, need regrow axons. We have shown regenerative models vivo vitro βB2-crystallin actively supports growth cut axons, thereby offering targets neuroprotective treatments. In this review we discuss discovery clearly regenerating retina vitro. βB2-Crystallin produced secreted during axon elongation, while promote acting either directly uptake into cells, or indirectly enhancing production ciliary neurotrophic factor astrocytes synergistically regrowth. methods induce continuous at site repair based on use transfected neural progenitor cells. This ultimately leads conclusion postinjury fate cannot seen merely inevitable, but instead should regarded shaping conditions cell