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Retinal degenerative diseases cause blindness characterized by a progressive decline in the number and function of retinal pigment epithelium (RPE), photoreceptor cells, and ganglion cells. Such diseases include retinitis pigmentosa (RP), glaucomatous optic neuropathy, age-related macular degeneration and diabetic optic neuropathy. Recent studies have demonstrated that Müller glial cells (MGCs), an endogenous alternative source of retinal neurons, are important glial cells involved in retinal development, damage, and regeneration, making it an excellent target for retinal nerve regeneration. Although hardly differentiate into neuron cells, transplanted MGCs have been shown to induce partial recovery of visual function in experimental retinal degenerative models. This improvement is possibly attributed to the release of neuroprotective factors that derived from the MGCs. With the development of the therapeutic usage of pluripotent stem cell, application of induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) originated derivation of MGCs have been widely used in retinal degenerative disease model such as glaucoma and retinitis pigmentosa model. This chapter summarized the relevant research and mechanisms and provided a broader application and research prospects for effective treatments in retinal degenerative diseases.
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http://dx.doi.org/10.1016/bs.pmbts.2023.03.026 | DOI Listing |
Zhonghua Yan Ke Za Zhi
September 2025
Beijing Tongren Eye Center, Beijing Institute of Ophthalmology, Beijing Ophthalmology&Visual Sciences Key Lab, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China.
Pathological myopia is one of the primary causes of irreversible visual loss in the population. Myopic maculopathy represents a key feature of pathological myopia, among which macular atrophy is the main contributor to severe visual impairment. The specific mechanism underlying the development of macular atrophy remains unclear.
View Article and Find Full Text PDFIEEE J Biomed Health Inform
September 2025
Retinal degenerative diseases such as age-related macular degeneration and retinitis pigmentosa cause severe vision impairment, while current electrical stimulation therapies are limited by poor spatial targeting precision. As a promising non-invasive alternative, the efficacy of temporal interference stimulation (TIS) for retinal targeting depends on optimized multi-electrode parameters. This study reconstructed a whole-head finite element model with detailed ocular structures and applied reinforcement learning (RL)-based multi-channel electrode parameter optimization to retinal stimulation.
View Article and Find Full Text PDFRetinal organoids (ROs) represent a promising regenerative strategy for restoring vision in retinal degenerative diseases, but whether host cone bipolar cells (BCs) in the primate macula can rewire with transplanted photoreceptors remains unresolved. Here, we transplanted genome-edited human retinal organoids lacking ON-BCs ( ROs) into a non-human primate macular degeneration model. Remarkably, host rod and cone BCs extended dendrites toward grafted photoreceptors, forming functional synapses confirmed by immunohistochemistry, ultrastructural imaging, and focal macular electroretinography.
View Article and Find Full Text PDFFront Ophthalmol (Lausanne)
August 2025
Aier Eye Institute, Changsha, China.
High myopia is a global health concern, often leading to degenerative retinal changes known as myopic retinopathy. Although mechanical stress, hypoperfusion, extracellular matrix remodeling, and growth factor dysregulation have been implicated in the pathogenesis of myopic retinopathy, emerging evidence highlights the critical role of chronic low-grade inflammation. Both innate and adaptive immune systems participate in myopic retinopathy through systemic and local inflammation.
View Article and Find Full Text PDFExp Eye Res
September 2025
Department of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou, China. Electronic address:
Retinitis pigmentosa (RP) is an inherited retinal degenerative disease characterized by progressive retinal pigment epithelium dysfunction and photoreceptor apoptosis, yet its pathogenesis remains unclear and no cure exists. Emerging evidence implicates the role of tryptophan metabolism in neuroinflammatory processes, prompting our investigation of serum tryptophan metabolites in RP patients versus healthy controls. Through targeted metabolomic profiling and clinical characterization, including age of onset, best corrected visual acuity (BCVA) and retinal thickness, we identified significant alterations in RP patients: marked decreases in cinnabarinic acid, xanthurenic acid, quinolinic acid and indole-3-carboxaldehyde (all p < 0.
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