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In the scholarly study, researchers showed that a rapid, sustained huge increase in eyes pressure in mice turns on a gene that activates a proteins known as caspase-8. This signaling proteins subsequently triggers the production of inflammatory proteins that normally help mammals combat microbial attacks. ‘This immune response is certainly a double-advantage sword because, while these proteins guard us from illness in a normal situation, they stimulate apoptosis in retinal cells in cases of severe glaucoma,’ said Zhang, who is also a staff doctor at the Veterans Affairs NORTH PARK Healthcare System. To confirm the mechanism linking high eye pressure to retinal harm further, researchers demonstrated that they could sluggish retinal cell death in mice with severe glaucoma by suppressing either the TLR4 gene or caspace-8 protein.