ArticleCell death & disease2018
Sphingosine kinase 1-associated autophagy differs between neurons and astrocytes.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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
26 citing papers in PubMed, 37 citations in OpenAlex.
- Sphingosine kinase 2 regulates protein ubiquitination networks in neurons.Molecular and cellular neurosciences · 2024Article
- Huntington's Disease: Complex Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024Review
- Herpes Simplex Virus type 1 inhibits autophagy in glial cells but requires ATG5 for the success of viral replication.Frontiers in microbiology · 2024Article
- The Tardigrade damage suppressor protein Dsup promotes DNA damage in neurons.Molecular and cellular neurosciences · 2023Article
- S1P Released by SGPL1-Deficient Astrocytes Enhances Astrocytic ATP Production via S1PRInternational journal of molecular sciences · 2023Article
- Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders.Nature reviews. Neuroscience · 2023Review
- The Emerging Role of Astrocytic Autophagy in Central Nervous System Disorders.Neurochemical research · 2022Article
- Impact of Aβ40 and Aβ42 Fibrils on the Transcriptome of Primary Astrocytes and Microglia.Biomedicines · 2022Article
- Ceramide/Sphingosine 1-Phosphate Axis as a Key Target for Diagnosis and Treatment in Alzheimer's Disease and Other Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Autophagy: Identification of MTMR5 as a neuron-enriched suppressor.Current biology : CB · 2022Article
- Review
- Research progress on astrocyte autophagy in ischemic stroke.Frontiers in neurology · 2022Review
- Modulation of the IGF1R-MTOR pathway attenuates motor neuron toxicity of human ALS SOD1Autophagy · 2021Article
- Article
- Differential responses of neurons, astrocytes, and microglia to G-quadruplex stabilization.Aging · 2021Article
- Regulation of autophagy by DNA G-quadruplexes.Autophagy · 2020Article
- Differential regulation of autophagy during metabolic stress in astrocytes and neurons.Autophagy · 2020Article
- Review
- On the relevance of precision autophagy flux controlAutophagy · 2020Article
- Small-molecule G-quadruplex stabilizers reveal a novel pathway of autophagy regulation in neurons.eLife · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Autophagy is a degradative pathway for removing aggregated proteins, damaged organelles, and parasites. Evidence indicates that autophagic pathways differ between cell types. In neurons, autophagy plays a homeostatic role, compared to a survival mechanism employed by starving non-neuronal cells. We investigated if sphingosine kinase 1 (SK1)-associated autophagy differs between two symbiotic brain cell types-neurons and astrocytes. SK1 synthesizes sphingosine-1-phosphate, which regulates autophagy in non-neuronal cells and in neurons. We found that benzoxazine autophagy inducers upregulate SK1 and neuroprotective autophagy in neurons, but not in astrocytes. Starvation enhances SK1-associated autophagy in astrocytes, but not in neurons. In astrocytes, SK1 is cytoprotective and promotes the degradation of an autophagy substrate, mutant huntingtin, the protein that causes Huntington's disease. Overexpressed SK1 is unexpectedly toxic to neurons, and its toxicity localizes to the neuronal soma, demonstrating an intricate relationship between the localization of SK1's activity and neurotoxicity. Our results underscore the importance of cell type-specific autophagic differences in any efforts to target autophagy therapeutically.
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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.