Changes in ganglioside GM1 expression in glaucomic retina

Pappenhagen, Nate; Inman, Denise M.

doi:10.1002/jnr.24273

Cited by 5 publications

(1 citation statement)

References 32 publications

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“…Both NGF and BDNF play neuroprotective roles in mouse models of glaucoma ( 272 , 273 , 274 ). Dysfunctional retinal ganglion cells stopped expressing GM1 in an animal model of glaucoma and this decreased expression may have affected the neuroprotective role played by NGF and BDNF ( 275 ). This finding supports a role for complex sphingolipids in glaucomic degeneration and identifies GM1 as a possible therapeutic target.…”

Section: Sphingolipids In Retinal Pathogenesismentioning

confidence: 99%

Sphingolipids as critical players in retinal physiology and pathology

Simón

Basu

Qaladize

et al. 2021

Journal of Lipid Research

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Sphingolipids have emerged as bioactive lipids involved in the regulation of many physiological and pathological processes. In the retina, they have been established to participate in numerous processes, such as neuronal survival and death, proliferation and migration of neuronal and vascular cells, inflammation, and neovascularization. Dysregulation of sphingolipids is, therefore, crucial in the onset and progression of retinal diseases. This review examines the involvement of sphingolipids in retinal physiology and diseases. Ceramide (Cer) emerges as a common mediator of inflammation and death of neuronal and retinal pigment epithelium cells in animal models of retinopathies such as glaucoma, age-related macular degeneration (AMD), and retinitis pigmentosa. Sphingosine-1-phosphate (S1P) has opposite roles, preventing photoreceptor and ganglion cell degeneration but also promoting inflammation, fibrosis, and neovascularization in AMD, glaucoma, and pro-fibrotic disorders. Alterations in Cer, S1P, and ceramide-1-phosphate may also contribute to uveitis. Notably, use of inhibitors that either prevent Cer increase or modulate S1P signaling, such as Myriocin, desipramine, and Fingolimod (FTY720), preserves neuronal viability and retinal function. These findings underscore the relevance of alterations in the sphingolipid metabolic network in the etiology of multiple retinopathies and highlight the potential of modulating their metabolism for the design of novel therapeutic approaches.

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