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Advanced Molecular Research on Retinopathy and Protection

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 September 2025 | Viewed by 1508

Special Issue Editor

Department of Ophthalmology and Visual Science, Eunpyeong St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea
Interests: retina; aged macular degeneration; diabetic retinopathy; retinal disease; retinal vascular disease

Special Issue Information

Dear Colleagues,

Retinopathy encompasses a range of retinal disorders characterized by damage to the retina, often resulting in vision impairment. Understanding the molecular mechanisms underlying different types of retinopathy is crucial for developing effective protective strategies. This research explores the pathophysiology, molecular targets, and potential interventions for several forms of retinopathy, including diabetic retinopathy, age-related macular degeneration (AMD), and various retinopathies.

Recent advancements in the protection and treatment of retinopathy focus on innovative therapies, lifestyle modifications, and emerging technologies. Ongoing research and innovations in pharmacotherapy, gene therapy, nutritional strategies, and lifestyle modifications are enhancing protection against various forms of retinopathy. These developments aim to improve patient outcomes and preserve vision through a multifaceted approach to prevention and treatment.

In addition to the content mentioned, studies related to retinopathy and protection are welcome for publication in this Special Issue. We hope that this Issue will contribute to the work of many researchers in the field.

Dr. Jaeyon Won
Guest Editor

Manuscript Submission Information

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Keywords

  • retinopathy
  • neuroprotection
  • antioxidants
  • innovative therapy
  • emerging technology

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Published Papers (1 paper)

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Research

12 pages, 10772 KiB  
Article
Quercetin Alleviates All-Trans-Retinal-Induced Photoreceptor Apoptosis and Retinal Degeneration by Inhibiting the ER Stress-Related PERK Signaling
by Bo Yang, Kunhuan Yang, Ruitong Xi, Jingmeng Chen and Yalin Wu
Int. J. Mol. Sci. 2024, 25(24), 13624; https://doi.org/10.3390/ijms252413624 - 19 Dec 2024
Viewed by 1114
Abstract
All-trans-retinal (atRAL)-induced photoreceptor atrophy and retinal degeneration are hallmark features of dry age-related macular degeneration (AMD) and Stargardt disease type 1 (STGD1). The toxicity of atRAL is closely related to the generation of reactive oxygen species (ROS). Quercetin, a natural product, [...] Read more.
All-trans-retinal (atRAL)-induced photoreceptor atrophy and retinal degeneration are hallmark features of dry age-related macular degeneration (AMD) and Stargardt disease type 1 (STGD1). The toxicity of atRAL is closely related to the generation of reactive oxygen species (ROS). Quercetin, a natural product, is known for its potent antioxidant properties; however, its effects in mitigating atRAL-mediated retinal damage remains unclear. This study investigated the protective effects of quercetin against atRAL-induced photoreceptor damage. Using atRAL-loaded 661W photoreceptor cells, we evaluated cell viability, ROS generation, and endoplasmic reticulum (ER) stress under quercetin treatment. Quercetin significantly restored the cell viability (to 70%) and reduced ROS generation in atRAL-treated 661W cells. Additionally, Western blot analysis demonstrated that quercetin mitigated protein kinase RNA-like ER kinase (PERK) signaling, preventing ER stress-induced apoptosis. Importantly, in Abca4−/−Rdh8−/− mice, an animal model of light-induced atRAL accumulation in the retina, quercetin treatment effectively alleviated light-exposed photoreceptor atrophy and retinal degeneration by attenuating PERK signaling. Thus, quercetin protected photoreceptor cells from atRAL-induced damage by inhibiting ROS generation and PERK signaling, which suggests its potential as a therapeutic agent for atRAL-related retinal degeneration. Full article
(This article belongs to the Special Issue Advanced Molecular Research on Retinopathy and Protection)
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