Neuroinflammation and Oxidative Stress in Retinal Neurodegeneration
This special issue belongs to the section "Cellular Neuroscience".
Special Issue Information
Dear Colleagues,
Retinal degeneration is a complex, multifactorial process driven by the interplay of neuroinflammation and oxidative stress, which together promote progressive neuronal loss. The retina is uniquely vulnerable due to its high metabolic demand, continuous exposure to light, and dependence on efficient mitochondrial function. Under pathological conditions, excessive production of reactive oxygen species (ROS) damages mitochondria, impairing energy metabolism, disturbing calcium homeostasis, and activating cell death pathways that ultimately compromise retinal survival.
Simultaneously, glial activation, particularly of Müller cells, microglia, and astrocytes, triggers a sustained inflammatory cascade that feeds forward to amplify oxidative stress and exacerbate neuronal dysfunction. This reciprocal relationship between redox imbalance and inflammation drives degeneration across multiple retinal cell types, including photoreceptors and retinal ganglion cells.
Unravelling the molecular crosstalk between oxidative and inflammatory pathways is now a critical priority for identifying transformative neuroprotective strategies. Therapeutic approaches are rapidly evolving and may involve antioxidant treatments, mitochondrial-targeted interventions, or the modulation of glial reactivity to restore retinal homeostasis and vision. Breakthroughs in this field hold the promise of delivering impactful, disease-modifying interventions to halt or even reverse vision loss in retinal degenerative diseases.
Dr. Hanhan Liu
Dr. Imre Lengyel
Dr. Pietro Bertelli
Guest Editors
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Keywords
- retinal degeneration
- oxidative stress
- neuroinflammation
- mitochondrial dysfunction
- gliosis
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