Purpose: To investigate the effects of a hereditary retinal degeneration on retinal oxygenation and determine whether it is responsible for the severe attenuation of retinal circulation in hereditary photoreceptor degenerations.
Methods: Seven adult Abyssinian cats affected by hereditary retinal degeneration were studied. Oxygen microelectrodes were used to collect spatial profiles of retinal oxygenation in anesthetized animals. A one-dimensional model of oxygen diffusion was fitted to the data to quantify photoreceptor oxygen utilization (Qo(2)).
Results: Photoreceptor Qo(2) progressively decreased until it reached zero in the end stage of the disease. Average inner retinal oxygen tension remained within normal limits at all disease stages, despite the observed progressive retinal vessel attenuation. Light affected photoreceptors normally, decreasing Qo(2) by approximately 50% at all stages of the disease.
Conclusions: Loss of photoreceptor metabolism allows choroidal oxygen to reach the inner retina, attenuating the retinal circulation in this animal model of retinitis pigmentosa (RP) and probably also in human RP. As the degeneration progresses, there is a strong relationship between changes in the a-wave of the ERG and changes in rod oxidative metabolism, indicating that these two functional measures change together.
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http://dx.doi.org/10.1167/iovs.05-1284 | DOI Listing |
Invest Ophthalmol Vis Sci
January 2025
Department of Ophthalmology, the First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, USTC, Hefei, China.
Purpose: Oxidative phosphorylation (OXPHOS) is an aerobic metabolic mechanism, and its dysfunction plays an important role in the pathological changes of ischemic diseases. However, systematic studies on the occurrence of retinal detachment (RD) are lacking.
Methods: Single-cell RNA sequencing (scRNA-seq) of the human retina was performed to detect the metabolic changes of various retinal cells after RD.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao
December 2024
Department of Neonatology, Children's Hospital of Nanjing Medical University,Nanjing 210000,China.
Objective To explore the role of the base mismatch repair gene Mutyh in retinopathy of prematurity(ROP). Methods Mutyh(-/-)and wild-type(WT)mice were used for the modeling of oxygen-induced retinopathy.The retinal oxidative stress was examined,and the ultrastructures of photoreceptors and mitochondria were observed.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Translational Neuroscience, Barrow Neurological Institute, St Joseph's Hospital and Medical Center (SJHMC), Phoenix, AZ 85013, USA.
Traumatic optic neuropathy (TON) has been regarded a vision-threatening condition caused by either ocular or blunt/penetrating head trauma, which is characterized by direct or indirect TON. Injury happens during sports, vehicle accidents and mainly in military war and combat exposure. Earlier, we have demonstrated that remote ischemic post-conditioning (RIC) therapy is protective in TON, and here we report that AMPKα1 activation is crucial.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Fujian Provincial Key Laboratory of Ophthalmology and Visual Science, Fujian Engineering and Research Center of Eye Regenerative Medicine, Eye Institute of Xiamen University, School of Medicine, Xiamen University, Xiamen 361102, China.
All--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.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Dipartimento di Biotecnologie e Scienze della Vita, ASST Sette Laghi, Università degli Studi dell'Insubria, 21100 Varese, Italy.
Hypertension exerts a profound impact on the microcirculation, causing both structural and functional alterations that contribute to systemic and organ-specific vascular damage. The microcirculation, comprising arterioles, capillaries, and venules with diameters smaller than 20 μm, plays a fundamental role in oxygen delivery, nutrient exchange, and maintaining tissue homeostasis. In the context of hypertension, microvascular remodeling and rarefaction result in reduced vessel density and elasticity, increasing vascular resistance and driving end-organ damage.
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