About this Research Topic
Retinal diseases are the most important causes of vision impairment in the working-age population and include inherited retina disorders (IRDs), e.g., retinitis pigmentosa (RP), Leber congenital amaurosis, Leber Hereditary Optic Neuropathy (LHON), and Autosomal Dominant Optic Atrophy (ADOA), and multifactorial conditions, e.g., Age-related Macular Degeneration (AMD), Diabetic Retinopathy (DR) and Glaucoma. The retina is the neuronal tissue in charge of visual function, organized in the Outer Retina (OR), composed by the photoreceptors and the Retina Pigment Epithelium (RPE), and Inner Retina (IR) layers, composed by the interneurons, bipolar cells, amacrine cells, horizontal cells, and retinal ganglion cells (RGCs). Besides neurons, the retina contains also a glial component, represented by Müller cells, astrocytes, and the microglia. Most retinal diseases can be categorized into those involving the death of photoreceptors and/or RPE in the OR, and those directly affecting neurons of the IR, usually RGCs. In this context, glial component cells orchestrate neuroinflammatory response, recovery from injury, and progression of disease.
The high genetic heterogeneity of retinal diseases highlights the need for identification of mutation-independent therapeutic strategies, aiming to minimize and/or delay cell loss in the diseased retina, as valid alternatives and/or complementary approaches to gene-replacement strategies. Moreover, targeting key effectors that impact commonly dysregulated pathways in neuronal damage during disease progression and aging holds great promise also as therapeutic options for dominant forms of inherited retina disorders and in multifactorial retinal diseases.
Although degeneration of retinal cells is the common landmark of these diseases, the underlying molecular and cellular events are still poorly understood. This Research Topic will provide greater insight into the mechanisms underlying retinal disease pathogenesis and progression, to identify possible early molecular and cellular events that could be targeted for therapeutic purposes. Contributors will provide more information about signaling pathways, and gene/mutation-therapeutic approaches in retinal degeneration.
The high genetic heterogeneity of retinal diseases highlights the need for identification of mutation-independent therapeutic strategies, aiming to minimize and/or delay cell loss in the diseased retina, as valid alternatives and/or complementary approaches to gene-replacement strategies. Moreover, targeting key effectors that impact commonly dysregulated pathways in neuronal damage during disease progression and aging holds great promise also as therapeutic options for dominant forms of inherited retina disorders and in multifactorial retinal diseases.
Although degeneration of retinal cells is the common landmark of these diseases, the underlying molecular and cellular events are still poorly understood. This Research Topic will provide greater insight into the mechanisms underlying retinal disease pathogenesis and progression, to identify possible early molecular and cellular events that could be targeted for therapeutic purposes. Contributors will provide more information about signaling pathways, and gene/mutation-therapeutic approaches in retinal degeneration.
Keywords: Retina;, neurodegeneration;, mutation-independent therapy;, molecular mechanism;, retinal diseases
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