ArticleCell death & disease2018
Phosphatidylserine is a marker for axonal debris engulfment but its exposure can be decoupled from degeneration.
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 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- An ApoE-Associated Low-Inflammatory Microglial State Emerges After Inflammatory Challenge in Alzheimer's Disease Mice.Neuroscience bulletin · 2026Article
- Loss of Atp8a2 drives neurodegeneration through the dysregulation of spatiotemporal phosphatidylserine externalization in mature neurons.Cell death & disease · 2026Article
- MerTK-triggered TGFβ1 autocrine signal regulates microglial response to neurodegeneration.Nature communications · 2026Article
- Microglia and immune signaling as architects of the brain.Frontiers in cellular neuroscience · 2026Review
- TDP-43 suppression of ATP8A2 cryptic splicing implicates phosphatidylserine-driven neuroinflammation in ALS/FTD.bioRxiv : the preprint server for biology · 2025Article
- Sigma-1 receptor activation by PRE-084 attenuates sepsis-associated encephalopathy by targeting microglial p38 MAPK-mediated neuroinflammation and neuronal endoplasmic reticulum stress.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Neuron-to-glia signaling drives critical period experience-dependent synapse pruning.Scientific reports · 2025Article
- Suppressing phagocyte activation by overexpressing the phosphatidylserine lipase ABHD12 preserves sarmopathic nerves.iScience · 2025Article
- Phagocytosis-driven neurodegeneration through opposing roles of an ABC transporter in neurons and phagocytes.Science advances · 2025Article
- Axonal spheroids are regulated by Schwann cells after peripheral nerve injury.bioRxiv : the preprint server for biology · 2024Article
- Microglia Gravitate toward Amyloid Plaques Surrounded by Externalized Phosphatidylserine via TREM2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Phospholipid scramblase Xkr8 is required for developmental axon pruning via phosphatidylserine exposure.The EMBO journal · 2023Article
- TheProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Actin-dependent astrocytic infiltration is a key step for axon defasciculation during remodeling.Cell reports · 2023Article
- Mast cell-derived BH4 is a critical mediator of postoperative pain.bioRxiv : the preprint server for biology · 2023Article
- A duplex structure of SARM1 octamers stabilized by a new inhibitor.Cellular and molecular life sciences : CMLS · 2022Article
- Macrophage depletion blocks congenital SARM1-dependent neuropathy.The Journal of clinical investigation · 2022Article
- Phenotypic drug screen uncovers the metabolic GCH1/BH4 pathway as key regulator of EGFR/KRAS-mediated neuropathic pain and lung cancer.Science translational medicine · 2022Article
- Microglia regulation of synaptic plasticity and learning and memory.Neural regeneration research · 2022Review
- Phagocytosis and self-destruction break down dendrites ofProceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptotic cells expose Phosphatidylserine (PS), that serves as an "eat me" signal for engulfing cells. Previous studies have shown that PS also marks degenerating axonsduring developmental pruning or in response to insults (Wallerian degeneration), but the pathways that control PS exposure on degenerating axons are largely unknown. Here, we used a series of in vitro assays to systematically explore the regulation of PS exposure during axonal degeneration. Our results show that PS exposure is regulated by the upstream activators of axonal pruning and Wallerian degeneration. However, our investigation of signaling further downstream revealed divergence between axon degeneration and PS exposure. Importantly, elevation of the axonal energetic status hindered PS exposure, while inhibition of mitochondrial activity caused PS exposure, without degeneration. Overall, our results suggest that the levels of PS on the outer axonal membrane can be dissociated from the degeneration process and that the axonal energetic status plays a key role in the regulation of PS exposure.
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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.