Diabetic retinopathy [Neurosurgery Wiki]

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====== Diabetic retinopathy ======

[[Retinal ganglion cell damage]] serves as a key indicator of various [[retina]]l [[degenerative disease]]s, including [[diabetic retinopathy]] (DR), [[glaucoma]], retinal arterial and retinal vein [[occlusion]]s, as well as inflammatory and traumatic optic neuropathies. Despite the growing body of data on the RGC [[proteomics]] associated with these conditions, there has been no dedicated study conducted to compare the molecular signaling pathways involved in the mechanism of neuronal cell death. Therefore, Starr et al. launched the study using two different insults leading to RGC death: glutamate [[excitotoxicity]] and optic nerve crush (ONC). C57BL/6 mice were used for the study and underwent NMDA- and ONC-induced damage. Twenty-four hours after ONC and 1 hour after NMDA injection, they collected RGCs using CD90.2 coupled magnetic beads, prepared protein extracts, and employed LC-MS for the global proteomic analysis of RGCs. Statistically significant changes in proteins were analyzed to identify changes to cellular signaling resulting from the treatment. They identified unique and common alterations in protein profiles in RGCs undergoing different types of cellular stresses. The study not only identified both unique and shared proteomic changes but also laid the groundwork for the future development of a therapeutic platform for testing gene candidates for DR and glaucoma
((Starr CR, Mobley JA, Gorbatyuk MS. Comparative Proteomic Study of Retinal Ganglion Cells Undergoing Various Types of Cellular Stressors. Exp Eye Res. 2024 Aug 8:110032. doi: 10.1016/j.exer.2024.110032. Epub ahead of print. PMID: 39127235.)).
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Visual [[impairment]] in [[diabetes]] is a growing [[public health]] concern. Apart from the well-defined diabetic [[retinopathy]], disturbed [[optic nerve]] function, which is dependent on the [[myelin sheath]], has recently been recognized as an early feature of visual impairment in diabetes. However, the underlying cellular mechanisms remain unclear. Using a [[streptozotocin]]-induced diabetic mouse model, Wu et al. observed a [[myelin]] deficiency along with a disturbed composition of [[oligodendroglia]]l lineage cells in the diabetic [[optic nerve]]. They found that new myelin deposition, a continuous process that lasts throughout adulthood, was diminished during [[pathogenesis]]. Genetically dampening newly generated myelin by conditionally deleting [[olig2]] in [[oligodendrocyte]] precursor cells within this short time window extensively delayed the signal transmission of the adult [[optic nerve]]. In addition, [[clemastine]], an antimuscarinic compound that enhances myelination, significantly restored oligodendroglia and promoted the functional recovery of the [[optic nerve]] in diabetic mice. The results point to the role of new [[myelin]] deposition in [[optic neuropathy]] under diabetic insult and provide a promising therapeutic target for restoring [[visual function]]
((Wu H, Chen X, Yu B, Zhang J, Gu X, Liu W, Mei F, Ye J, Xiao L. Deficient deposition of new [[myelin]] impairs adult [[optic nerve]] function in a murine model of diabetes. Glia. 2023 Jan 20. doi: 10.1002/glia.24341. Epub ahead of print. PMID: 36661098.))