ArticleJournal of immunology (Baltimore, Md. : 1950)2013
SARM is required for neuronal injury and cytokine production in response to central nervous system viral infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 61 citations in OpenAlex.
- Caspase-3 cleaves and activates the NADase SARM1 to promote apoptosis, linking two cell death mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections.Journal of neuroinflammation · 2025Article
- Inhibition of SARM1 Reduces Neuropathic Pain in a Spared Nerve Injury Rodent Model.Muscle & nerve · 2025Article
- SARM regulates cell apoptosis and inflammation during Toxoplasma gondii infection through a multistep mechanism.Parasites & vectors · 2025Article
- SARM1 in the pathogenesis of immune-related disease.Toxicology research · 2024Review
- Erdr1 Drives Macrophage Programming via Dynamic Interplay with YAP1 and Mid1.ImmunoHorizons · 2024Article
- Genetic ablation of Sarm1 attenuates expression and mislocalization of phosphorylated TDP-43 after mouse repetitive traumatic brain injury.Acta neuropathologica communications · 2023Article
- Erdr1 orchestrates macrophage polarization and determines cell fate via dynamic interplay with YAP1 and Mid1.bioRxiv : the preprint server for biology · 2023Article
- Astrocytic SARM1 promotes neuroinflammation and axonal demyelination in experimental autoimmune encephalomyelitis through inhibiting GDNF signaling.Cell death & disease · 2022Article
- SARM suppresses TRIF, TRAF3, and IRF3/7 mediated antiviral signaling in large yellow croakerFrontiers in immunology · 2022Article
- SARM1 Suppresses Axon Branching Through Attenuation of Axonal Cytoskeletal Dynamics.Frontiers in molecular neuroscience · 2022Article
- A Novel NAD Signaling Mechanism in Axon Degeneration and its Relationship to Innate Immunity.Frontiers in molecular biosciences · 2021Review
- NADFrontiers in molecular biosciences · 2021Review
- Article
- Passenger Mutations Confound Phenotypes of SARM1-Deficient Mice.Cell reports · 2020Article
- Programmed axon degeneration: from mouse to mechanism to medicine.Nature reviews. Neuroscience · 2020Review
- Pathological modeling of TBEV infection reveals differential innate immune responses in human neurons and astrocytes that correlate with their susceptibility to infection.Journal of neuroinflammation · 2020Article
- Sarm1 knockout protects against early but not late axonal degeneration in experimental allergic encephalomyelitis.PloS one · 2020Article
- SARM1 deficiency up-regulates XAF1, promotes neuronal apoptosis, and accelerates prion disease.The Journal of experimental medicine · 2019Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Four of the five members of the Toll/IL-1R domain-containing adaptor family are required for signaling downstream of TLRs, promoting innate immune responses against different pathogens. However, the role of the fifth member of this family, sterile α and Toll/IL-1R domain-containing 1 (SARM), is unclear. SARM is expressed primarily in the CNS where it is required for axonal death. Studies in Caenorhabditis elegans have also shown a role for SARM in innate immunity. To clarify the role of mammalian SARM in innate immunity, we infected SARM(-/-) mice with a number of bacterial and viral pathogens. SARM(-/-) mice show normal responses to Listeria monocytogenes, Mycobacterium tuberculosis, and influenza virus, but show dramatic protection from death after CNS infection with vesicular stomatitis virus. Protection correlates with reduced CNS injury and cytokine production by nonhematopoietic cells, suggesting that SARM is a positive regulator of cytokine production. Neurons and microglia are the predominant source of cytokines in vivo, supporting a role for SARM as a link between neuronal injury and innate immunity.
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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.