ReviewNeurochemical research2011
Secondary alterations of sphingolipid metabolism in lysosomal storage diseases.
Review in Neurochemical research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Metabolic and Structural Consequences of GM3 Synthase Deficiency: Insights from an HEK293-T Knockout Model.Biomedicines · 2025Article
- Granulins rescue inflammation, lysosome dysfunction, lipofuscin, and neuropathology in a mouse model of progranulin deficiency.Cell reports · 2024Article
- Plasma membrane glycosphingolipid signaling: a turning point.Glycoconjugate journal · 2022Article
- A kaleidoscopic view of extracellular vesicles in lysosomal storage disorders.Extracellular vesicles and circulating nucleic acids · 2022Review
- Renal involvement in a patient with the chronic visceral subtype of acid sphingomyelinase deficiency resembles Fabry disease.JIMD reports · 2021Article
- Article
- Gangliosides in the differentiation process of primary neurons: the specific role of GM1-oligosaccharide.Glycoconjugate journal · 2020Article
- The oligosaccharide portion of ganglioside GM1 regulates mitochondrial function in neuroblastoma cells.Glycoconjugate journal · 2020Article
- GM1 Ganglioside Is A Key Factor in Maintaining the Mammalian Neuronal Functions Avoiding Neurodegeneration.International journal of molecular sciences · 2020Review
- Parkinson's disease recovery by GM1 oligosaccharide treatment in the B4galnt1Scientific reports · 2019Article
- The Neuroprotective Role of the GM1 Oligosaccharide, IIMolecular neurobiology · 2019Article
- A lysosome-plasma membrane-sphingolipid axis linking lysosomal storage to cell growth arrest.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Sensorimotor and Neurocognitive Dysfunctions Parallel Early Telencephalic Neuropathology in Fucosidosis Mice.Frontiers in behavioral neuroscience · 2018Article
- Pharmaceutical Chaperones and Proteostasis Regulators in the Therapy of Lysosomal Storage Disorders: Current Perspective and Future Promises.Frontiers in pharmacology · 2017Review
- Port-to-port delivery: Mobilization of toxic sphingolipids via extracellular vesicles.Journal of neuroscience research · 2016Article
- ASMase regulates autophagy and lysosomal membrane permeabilization and its inhibition prevents early stage non-alcoholic steatohepatitis.Journal of hepatology · 2014Article
- ASMase is required for chronic alcohol induced hepatic endoplasmic reticulum stress and mitochondrial cholesterol loading.Journal of hepatology · 2013Article
- The cell biology of disease: lysosomal storage disorders: the cellular impact of lysosomal dysfunction.The Journal of cell biology · 2012Review
- Mucopolysaccharidosis type I: current knowledge on its pathophysiological mechanisms.Metabolic brain disease · 2012Review
- Cathepsin B overexpression due to acid sphingomyelinase ablation promotes liver fibrosis in Niemann-Pick disease.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In several neurodegenerative diseases, sphingolipid metabolism is deeply deregulated, leading to the expression of abnormal membrane sphingolipid patterns and altered plasma membrane organization. In this paper, we review the potential importance of these alterations to the pathogenesis of these diseases and focus the reader's attention on some secondary alterations of sphingolipid metabolism that have been sporadically reported in the literature. Moreover, we present a detailed analysis of the lipid composition of different central nervous system and extraneural tissues from the acid sphingomyelinase-deficient mouse, the animal model for Niemann-Pick disease type A, characterized by the accumulation of sphingomyelin. Our data show an unexpected, tissue specific selection of the accumulated molecular species of sphingomyelin, and an accumulation of GM3 and GM2 gangliosides in both neural and extraneural tissues, that cannot be solely explained by the lack of acid sphingomyelinase.
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What OpenQuestion holds
Registered trials
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.