ArticlePloS one2015
Lack of Acid Sphingomyelinase Induces Age-Related Retinal Degeneration.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- The role of autophagy in ocular health: mechanisms, pathologies, and therapeutic strategies.Biology direct · 2026Pooled it
- Stratification of the Extent of Visual Impairment Identifies Sex-Specific Degenerative Changes in Retinal Structure and Function during Aging.Journal of integrative neuroscience · 2025Article
- Sphingolipid Levels and Processing of the Retinyl Chromophore in the Retina of a Mouse Model of Niemann-Pick Disease.Investigative ophthalmology & visual science · 2024Article
- Sphingomyelinases in retinas and optic nerve heads: Effects of ocular hypertension and ischemia.Experimental eye research · 2022Article
- Autophagy in the retinal pigment epithelium: a new vision and future challenges.The FEBS journal · 2022Review
- Evaluation of sphingolipid metabolism on diabetic retinopathy.Indian journal of ophthalmology · 2021Article
- Evidence for ceramide induced cytotoxicity in retinal ganglion cells.Experimental eye research · 2021Article
- Macula halo syndrome.International ophthalmology · 2019Article
- Acid Ceramidase Deficiency in Mice Leads to Severe Ocular Pathology and Visual Impairment.The American journal of pathology · 2019Article
- Sphingolipids as Emerging Mediators in Retina Degeneration.Frontiers in cellular neuroscience · 2019Review
- Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Suppression of Acid Sphingomyelinase Protects the Retina from Ischemic Injury.Investigative ophthalmology & visual science · 2016Article
- Targeting Lipid Metabolism for the Treatment of Age-Related Macular Degeneration: Insights from Preclinical Mouse Models.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and TherapeuticsReview
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMutations of acid sphingomyelinase (ASMase) cause Niemann-Pick diseases type A and B, which are fatal inherited lipid lysosomal storage diseases, characterized with visceral organ abnormalities and neurodegeneration. However, the effects of suppressing retinal ASMase expression are not understood. The goal of this study was to determine if the disruption of ASMase expression impacts the retinal structure and function in the mouse, and begin to investigate the mechanisms underlying these abnormalities.
methodsAcid sphingomyelinase knockout (ASMase KO) mice were utilized to study the roles of this sphingolipid metabolizing enzyme in the retina. Electroretinogram and morphometric analysis were used to assess the retinal function and structure at various ages. Sphingolipid profile was determined by liquid chromatography-mass spectrometry. Western blots evaluated the level of the autophagy marker LC3-II.
resultsWhen compared to control animals, ASMase KO mice exhibited significant age-dependent reduction in ERG a- and b-wave amplitudes. Associated with these functional deficits, morphometric analysis revealed progressive thinning of retinal layers; however, the most prominent degeneration was observed in the photoreceptor and outer nuclear layer. Additional analyses of ASMase KO mice revealed early reduction in ERG c-wave amplitudes and increased lipofuscin accumulation in the retinal pigment epithelium (RPE). Sphingolipid analyses showed abnormal accumulation of sphingomyelin and sphingosine in ASMase KO retinas. Western blot analyses showed a higher level of the autophagosome marker LC3-II.
conclusionsThese studies demonstrate that ASMase is necessary for the maintenance of normal retinal structure and function. The early outer retinal dysfunction, outer segment degeneration, accumulation of lipofuscin and autophagosome markers provide evidence that disruption of lysosomal function contributes to the age-dependent retinal degeneration exhibited by ASMase KO mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.