[Role of Heat Shock Protein 70 in Retinitis Pigmentosa and a Novel Strategy for Treatment].

Retinitis pigmentosa (RP) is a group of inherited disorders involving the photoreceptors of the retina and can lead to visual loss. There has been tremendous progress in the delineation of the biochemical and molecular basis of RP. Reactive oxygen species, calcium-calpain activation, and lipid peroxidation are known to be involved in the initiation of photoreceptor cell death, but the precise mechanisms of this process remain unknown. Heat shock protein 70 (HSP70) has been shown to function as a chaperone molecule that protects cells against environmental and physiological stresses. However, there are a few reports showing the role of HSP70 in photoreceptor cell death. Recently, we found that the production of 4-hydroxy-2-noneral caused the calpain-dependent cleavage of carbonylated HSP70 prior to photoreceptor cell death in RP model mice. Furthermore, HSP70 inducers, such as valproic acid and geranylgeranylacetone attenuated photoreceptor cell death. HSP70 inducers may be considered as candidate therapeutic agents for RP.