In vivo retinal melanin detection with the calibrated depolarization index in polarization-sensitive optical coherence tomography DOI Creative Commons
Mengyuan Ke, Liqin Jiang, Veluchamy A. Barathi

и другие.

Journal of Biomedical Optics, Год журнала: 2024, Номер 29(12)

Опубликована: Дек. 19, 2024

SignificanceA data-based calibration method with enhanced depolarization contrast in polarization-sensitive optical coherence tomography (PS-OCT) was developed and demonstrated effective for detecting melanin content the eye.AimWe aim to mitigate dependence between measured metric intensity signal-to-noise ratio (SNR) improved visualization of depolarizing tissues, especially low SNR regions, demonstrate evaluate presence.ApproachA function calibrating experimentally derived from young albino guinea pig, assuming free retina. A longitudinal study pigs (9 weeks) conducted assess accumulation during early eye growth. Furthermore, sub-macular choroid compared eyes light dark irides involving 14 human subjects middle adulthood.ResultsWe observed an increase contrast, which indicates potential development age pigmented pig eyes. We found a significant difference colors.ConclusionsOur proposed structures PS-OCT, can be generalized all kinds imaging potentially monitor healthy pathological

Язык: Английский

Sodium Iodate-Induced Ferroptosis in Photoreceptor-Derived 661W Cells Through the Depletion of GSH DOI Open Access
Chao Chen, Han Wang,

Jiuyu Yang

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(5), С. 2334 - 2334

Опубликована: Март 5, 2025

Oxidative stress-induced photoreceptor cell death is closely associated with the etiology of age-related macular degeneration (AMD), and sodium iodate (SI) has been widely used as an oxidant stimulus in AMD models to induce retinal pigment epithelium (RPE) death. However, mechanism underlying SI-induced remains controversial unclear. In this study, we elucidate that ferroptosis a critical form induced by SI photoreceptor-derived 661W cells. disrupts system Xc-, leading glutathione (GSH) depletion triggering lipid peroxidation, thereby promoting Additionally, enhances intracellular Fe2+ levels, which further facilitates reactive oxygen species (ROS) accumulation, making cells more susceptible ferroptosis. Exogenous GSH, well specific inhibitors such Fer-1 antioxidants like NAC, significantly attenuate These findings provide new insights into mechanisms key pathway

Язык: Английский

Процитировано

0

The role of retinal pigment epithelial senescence and the potential of senotherapeutics in age-related macular degeneration DOI
Yingying Chen,

Feipeng Jiang,

Yue Zeng

и другие.

Survey of Ophthalmology, Год журнала: 2025, Номер unknown

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

0

Illuminating eye care: the promise and future of red light therapy in ophthalmology DOI
Fei Xue, Yating Zhou

Graefe s Archive for Clinical and Experimental Ophthalmology, Год журнала: 2025, Номер unknown

Опубликована: Март 19, 2025

Язык: Английский

Процитировано

0

Therapeutic Potential of Hexahydrocurcumin in the Regeneration and Protection of the Retinal Pigment Epithelium DOI Creative Commons
Ilona Nowak, Robert Kubina, Barbara Strzałka‐Mrozik

и другие.

Pharmaceuticals, Год журнала: 2025, Номер 18(4), С. 554 - 554

Опубликована: Апрель 9, 2025

Hexahydrocurcumin (HHC), the primary metabolite of curcumin, shows promising therapeutic potential due to its antioxidant and anti-inflammatory properties. The retinal pigment epithelium (RPE) plays a crucial role in maintaining homeostasis; however, dysfunction—linked oxidative stress chronic inflammation—contributes progression degenerative diseases such as age-related macular degeneration (AMD). This review highlights HHC protecting regenerating RPE cells. It explores effects on RPE, mechanisms underlying damage, involvement reactive oxygen species (ROS) inflammatory mediators. has demonstrated ability modulate these pathways by activating nuclear factor erythroid 2-related 2 (NRF2), enhancing defenses, inhibiting pro-inflammatory cytokine production. Preclinical studies suggest that mitigates vascular remodeling endothelial dysfunction reducing expression transforming growth β (TGF-β1) matrix metalloproteinase-9 (MMP-9). Moreover, improves nitric oxide bioavailability promotes synthase expression, thereby counteracting stress-induced damage. Emerging evidence indicates may be candidate for treatment diseases, particularly those associated with inflammation. However, further studies, including clinical trials, are essential confirm efficacy elucidate precise HHC’s protective

Язык: Английский

Процитировано

0

Exploring Retinal Conditions Through Blue Light Reflectance Imaging DOI
Ricardo Luz Leitão Guerra,

Cezar Luz Leitão Guerra,

Mariana Gouveia Bastos Meirelles

и другие.

Progress in Retinal and Eye Research, Год журнала: 2025, Номер 105, С. 101326 - 101326

Опубликована: Янв. 5, 2025

Язык: Английский

Процитировано

0

Tyrosol protects RPE cells from H2O2-induced oxidative damage in vitro and in vivo through activation of the Nrf2/HO-1 pathway DOI
Longtai You, Wenwen Zhao, Li Xiao

и другие.

European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177316 - 177316

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

0

Capilliposide A relieved dry age-related macular degeneration through ROS/SIRT1/P53 signaling pathway DOI

Fanwei Xia,

Luping Wang,

Ying Ji

и другие.

European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177412 - 177412

Опубликована: Фев. 1, 2025

Язык: Английский

Процитировано

0

Melatonin protects retinal pigment epithelium cells against ferroptosis in AMD via the PI3K/AKT/MDM2/P53 pathway DOI Creative Commons

Ping Wu,

Long Zhao, Yong Du

и другие.

Frontiers in Pharmacology, Год журнала: 2025, Номер 16

Опубликована: Фев. 27, 2025

Oxidative stress-prompted degeneration of the retinal pigment epithelium (RPE) notably contributes to onset age-related macular (AMD). However, pathways leading RPE deterioration and possible preventative strategies are not yet completely comprehended. Ferroptosis was assayed through evaluation lipid peroxidation (C11-BODIPY MDA), reactive oxygen species (ROS), transmission electron microscopy (TEM), iron content measurement, q-PCR, western blotting, immunofluorescence. To assess structure function in mice, ERG (electroretinography), OCT (optical coherence tomography), H&E (hematoxylin eosin) staining were employed. Network pharmacology methods utilized elucidate potential mechanisms underlying melatonin's protective effects against ferroptosis cells AMD. Genetic engineering techniques applied investigate regulatory relationships among phosphatidylinositol 3-kinase (PI3K), protein kinase-B (AKT), murine double minute-2 (MDM2), 53 (P53), solute carrier family 7 member 11 (SLC7A11). In vitro knockdown experiments MDM2 conducted explore its role within cells. Aβ1-40 can trigger Melatonin inhibit oxidative stress induced by exhibits a effect on Aβ1-40-induced AMD, significantly improving mouse retina layer, facilitating restoration visual function. revealed that targets melatonin AMD closely related ferroptosis, indicated predominant associated with PI3K/AKT/MDM2/P53 signaling pathway. Knocking down specific expression weaken inhibitory ferroptosis. suppress cell death via pathway, thereby preventing decelerating progression

Язык: Английский

Процитировано

0

Preserving blood-retinal barrier integrity: a path to retinal ganglion cell protection in glaucoma and traumatic optic neuropathy DOI Creative Commons

Lai-Yang Zhou,

Zhen-Gang Liu,

Sun Yong-quan

и другие.

Cell Regeneration, Год журнала: 2025, Номер 14(1)

Опубликована: Апрель 2, 2025

Retinal ganglion cells (RGCs) are the visual gateway of brain, with their axons converging to form optic nerve, making them most vulnerable target in diseases such as glaucoma and traumatic neuropathy (TON). In both diseases, disruption blood-retinal barrier(BRB) is considered an important mechanism that accelerates RGC degeneration hinders axon regeneration. The BRB consists inner barrier (iBRB) outer (oBRB), which maintained by endothelial cells(ECs), pericytes(PCs), retinal pigment epithelial (RPE), respectively. Their functions include regulating nutrient exchange, oxidative stress, immune microenvironment. However, TON, structural functional integrity severely damaged due mechanical inflammatory reactions, metabolic disorders. Emerging evidence highlights leads heightened vascular permeability, cell infiltration, sustained chronic inflammation, creating a hostile microenvironment for survival. Furthermore, dynamic interplay imbalance among ECs, PCs, glial within neurovascular unit (NVU) pivotal drivers destruction, exacerbating apoptosis limiting nerve intricate molecular cellular mechanisms underlying these processes underscore BRB's critical role TON pathophysiology while offering compelling foundation therapeutic strategies targeting repair stabilization. This review provides crucial insights lays robust groundwork advancing research on neural regeneration innovative protective strategies.

Язык: Английский

Процитировано

0

The role of peripheral blood microRNAs in the pathogenesis and treatment response of age-related macular degeneration DOI Creative Commons
Meng Kong,

Jingwen Li,

Nianting Tong

и другие.

Future Science OA, Год журнала: 2025, Номер 11(1)

Опубликована: Апрель 4, 2025

Age-related macular degeneration is a leading cause of vision loss in aging populations, driven by complex interactions between genetic, environmental, and molecular factors. MicroRNAs have emerged as crucial regulators cellular processes such oxidative stress, inflammation, angiogenesis, all which contribute to AMD pathogenesis. This narrative review aims summarize the involvement peripheral blood microRNAs pathogenesis AMD, focusing on key pathways angiogenesis. Additionally, it explores their potential biomarkers for predicting treatment response, particularly anti-VEGF therapies. The miRNAs noninvasive early diagnosis personalized strategies also explored, highlighting future directions research.

Язык: Английский

Процитировано

0