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Secretogranin III: a promising therapeutic target for intraocular neovascular lesions.
Int Ophthalmol
January 2025
Department of Ophthalmology, The Second Hospital of Jilin University, #218 Ziqiang Street, Changchun, 130041, Jilin, China.
Purpose: The purpose of this study is to investigate the role of Secretogranin III (Scg3) in the pathogenesis of intraocular neovascular diseases and assess its potential as a therapeutic target for novel treatment strategies.
Methods: A literature review was conducted to examine the expression of Scg3 in intraocular neovascular diseases. We reviewed studies on the interaction of Scg3 with its homologous receptors and its effect on endothelial cell proliferation, migration, and vascular permeability-key processes involved in angiogenesis and neovascularization.
Autophagy serves as a protective effect against inflammatory injury of oxidative stress in ARPE-19 cell.
Int J Ophthalmol
January 2025
Department of Ophthalmology, the First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu Province, China.
Aim: To test the effect of autophagy on inflammatory damage resulting from oxidative stress in adult retinal pigment epithelial cell line (ARPE-19).
Methods: ARPE-19 cells were pretreated with 200 and 600 µmol/L hydrogen peroxide (HO) at various time intervals. The changes of cell morphology, cell viability, reactive oxygen species (ROS) level, autophagic activity, and the inflammatory cytokines (TNFα, IL-6, and TGFβ) were measured at baseline and after treatment with autophagy inducer rapamycin (Rapa) and suppressor wortmannin (Wort) or shATG5.
IL-17A mediates inflammation-related retinal pigment epithelial cells injury ERK signaling pathway.
Int J Ophthalmol
January 2025
Department of Ophthalmology, Shanghai General Hospital (Shanghai First People's Hospital), Shanghai Jiao Tong University, School of Medicine, Shanghai 200080, China.
Aim: To investigate whether interleukin-17A (IL-17A) gets involved in the mechanisms of inflammation-related retinal pigment epithelium (RPE) cells injury and its significance in age-related macular degeneration (AMD).
Mrthods: A sodium iodate (NaIO) mouse model as well as mice were established. The effects of inflammatory cytokines in RPE cells and retinal microglia before and after NaIO modeling and , were investigated using immunofluorescence, immunoprotein blotting, and quantitative real-time fluorescence polymerase chain reaction (qRT-PCR), respectively.
Exploring causal relationships between immune cells and age-related macular degeneration through univariable, bidirectional, and multivariable Mendelian analysis.
Front Med (Lausanne)
December 2024
Department of Ophthalmology, Children's Hospital of Fudan University Xiamen Branch, Xiamen Children's Hospital, Xiamen, China.
Objective: This study systematically investigates the causal relationships between 731 immune cell phenotypes and age-related macular degeneration (AMD) using comprehensive Mendelian randomization (MR) analyses. The goal is to identify immune cell factors that contribute to or protect against AMD, thereby clarifying the immunological mechanisms underlying AMD pathophysiology and informing prevention and treatment strategies.
Methods: Univariable, bidirectional, and multivariable MR analyses were conducted to evaluate the associations between immune cells and AMD.
Extracellular Mitochondria Exacerbate Retinal Pigment Epithelium Degeneration in Diabetic Retinopathy.
Diabetes
December 2024
Department of Ophthalmology and Visual Sciences, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Article Synopsis
- Advances in fundus imaging are uncovering disruptions in the neurovascular unit related to diabetic retinopathy (DR), highlighting the need for a better understanding of neurodegeneration during anti-VEGF treatments.
- Extracellular mitochondria are found to worsen retinal pigment epithelium (RPE) degeneration and inflammation in DR patients by increasing in the vitreous and are linked with visual impairment, but not other advanced retinopathy complications.
- The study reveals that these mitochondria trigger cell death in RPE cells via a process dependent on mitochondrial DNA and induce inflammatory responses through specific receptors, positioning them as a critical factor in the worsening of RPE deterioration in DR.
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