ArticleStem cells (Dayton, Ohio)2016
Role of Acid Sphingomyelinase in Shifting the Balance Between Proinflammatory and Reparative Bone Marrow Cells in Diabetic Retinopathy.
Article in Stem cells (Dayton, Ohio), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 47 citations in OpenAlex.
- Lipid homeostasis plays a critical role in inherited and acquired retinal diseases.Communications biology · 2026Review
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
- Lipidomic analysis of vitreous humor derived from patients with proliferative diabetic retinopathy.BMC ophthalmology · 2025Article
- Causal role of plasma liposome in diabetic retinopathy: mendelian randomization (MR) study.Diabetology & metabolic syndrome · 2025Article
- Elevated Very-Long-Chain Ceramides in the Vitreous Humor of Patients With Proliferative Diabetic Retinopathy.Investigative ophthalmology & visual science · 2025Article
- Diabetic retinopathy is a ceramidopathy reversible by anti-ceramide immunotherapy.Cell metabolism · 2024Article
- Common mechanisms underlying diabetic vascular complications: focus on the interaction of metabolic disorders, immuno-inflammation, and endothelial dysfunction.Cell communication and signaling : CCS · 2023Review
- Perilipin 2-positive mononuclear phagocytes accumulate in the diabetic retina and promote PPARγ-dependent vasodegeneration.The Journal of clinical investigation · 2023Article
- Regulation of serine palmitoyl-transferase and Rac1-Nox2 signaling in diabetic retinopathy.Scientific reports · 2022Article
- Lipids, hyperreflective crystalline deposits and diabetic retinopathy: potential systemic and retinal-specific effect of lipid-lowering therapies.Diabetologia · 2022Review
- Circulating inflammatory monocytes oppose microglia and contribute to cone cell death in retinitis pigmentosa.PNAS nexus · 2022Article
- Integrative biology of extracellular vesicles in diabetes mellitus and diabetic complications.Theranostics · 2022Review
- Evaluation of sphingolipid metabolism on diabetic retinopathy.Indian journal of ophthalmology · 2021Article
- Ceramide-mediation of diffusion in supported lipid bilayers.Chemistry and physics of lipids · 2021Article
- Alpha-mangostin improves endothelial dysfunction in db/db mice through inhibition of aSMase/ceramide pathway.Journal of cellular and molecular medicine · 2021Article
- Role of ceramides in the pathogenesis of diabetes mellitus and its complications.Journal of diabetes and its complications · 2021Review
- Multiplatform Metabolomics Reveals Novel Serum Metabolite Biomarkers in Diabetic Retinopathy Subjects.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Diabetic photoreceptors: Mechanisms underlying changes in structure and function.Visual neuroscience · 2020Review
- Selective LXR agonist DMHCA corrects retinal and bone marrow dysfunction in type 2 diabetes.JCI insight · 2020Article
- Extracellular Vesicle-Induced Classical Complement Activation Leads to Retinal Endothelial Cell Damage via MAC Deposition.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
The metabolic insults associated with diabetes lead to low-grade chronic inflammation, retinal endothelial cell damage, and inadequate vascular repair. This is partly due to the increased activation of bone marrow (BM)-derived proinflammatory monocytes infiltrating the retina, and the compromised function of BM-derived reparative circulating angiogenic cells (CACs), which home to sites of endothelial injury and foster vascular repair. We now propose that a metabolic link leading to activated monocytes and dysfunctional CACs in diabetes involves upregulation of a central enzyme of sphingolipid signaling, acid sphingomyelinase (ASM). Selective inhibition of ASM in the BM prevented diabetes-induced activation of BM-derived microglia-like cells and normalized proinflammatory cytokine levels in the retina. ASM upregulation in diabetic CACs caused accumulation of ceramide on their cell membrane, thereby reducing membrane fluidity and impairing CAC migration. Replacing sphingomyelin with ceramide in synthetic membrane vesicles caused a similar decrease in membrane fluidity. Inhibition of ASM in diabetic CACs improved membrane fluidity and homing of these cells to damaged retinal vessels. Collectively, these findings indicate that selective modulation of sphingolipid metabolism in BM-derived cell populations in diabetes normalizes the reparative/proinflammatory cell balance and can be explored as a novel therapeutic strategy for treating diabetic retinopathy.
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Registered trials
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