Age-related macular degeneration (AMD) is a significant cause of blindness in older adults, but the initial molecular changes that lead to vision loss are not well understood.
Research using sodium iodate (NaIO) on mice showed increased levels of the stress response protein REDD1 in the retina, which correlates with heightened oxidative stress and inflammation when NaIO is administered.
Mice without REDD1 experienced less damage, including reduced oxidative stress and preserved retinal structure, suggesting that REDD1 plays a crucial role in developing retinal issues associated with dry AMD.
This study investigates how diabetes triggers the activation of the NLRP3 inflammasome, a key player in retinal complications associated with diabetes.
Researchers found that both NLRP3 and interleukin-1β (IL-1β) levels increased in diabetic mice and cultured Müller cells under hyperglycemic conditions, with the stress response protein REDD1 being essential for this increase.
The findings suggest that REDD1 influences GSK3β activity, which is crucial for NLRP3 inflammasome activation and IL-1β production in Müller glial cells during diabetes, potentially affecting visual function in diabetic mice.
Inflammation plays a significant role in the development and progression of diabetic retinal complications, with REDD1 being a key protein involved in this process.
REDD1 promotes the activation of NF-κB, a transcription factor linked to inflammation, by affecting the phosphorylation of GSK3β, particularly under hyperglycemic conditions.
Inhibiting GSK3β in diabetic models can reduce NF-κB activity and pro-inflammatory cytokine expression, suggesting potential therapeutic avenues for managing diabetic retinal inflammation.
Inflammation in the retina is worsened by diabetes, and the study investigates the role of a stress response protein called REDD1 in this process.
Increased levels of REDD1 were found in the retinas of diabetic mice, and it was essential for the expression of inflammatory cytokines.
Deleting REDD1 in human retinal cells inhibited these cytokines by affecting the NF-κB signaling pathway, demonstrating that REDD1 is a key player in diabetic retinal inflammation.