ArticleJournal of immunology (Baltimore, Md. : 1950)2015
SARM1, Not MyD88, Mediates TLR7/TLR9-Induced Apoptosis in Neurons.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 67 citations in OpenAlex.
- Review
- 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
- Hyperglycemia promotes SIRT3-mediated deacetylation of SARM1 to exacerbate diabetic peripheral neuropathy in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- MicroRNA-29a-5p contributes to neuroinflammation through TLR7.Journal of neuroinflammation · 2026Article
- Evolutionarily ancient functions of enzymatic TIR proteins in innate immunity.Trends in immunology · 2025Review
- Transcranial Magnetic Stimulation Alleviates Spatial Learning and Memory Impairment by Inhibiting the Expression of SARM1 in Rats with Cerebral Ischemia-Reperfusion Injury.Neuromolecular medicine · 2025Article
- Neurodegenerative disease-associated microRNAs acting as signaling molecules modulate CNS neuron structure and viability.Cell communication and signaling : CCS · 2025Article
- SARM regulates cell apoptosis and inflammation during Toxoplasma gondii infection through a multistep mechanism.Parasites & vectors · 2025Article
- Toll-1-dependent immune evasion induced by fungal infection leads to cell loss in the Drosophila brain.PLoS biology · 2025Article
- Pharmacological and bioactive properties ofFrontiers in pharmacology · 2025Review
- Retinoic acid-induced differentiation and oxidative stress inhibitors increase resistance of human neuroblastoma cells to La Crosse virus-induced cell death.Journal of virology · 2024Article
- The Role of NMNAT2/SARM1 in Neuropathy Development.Biology · 2024Review
- The Sixth Sense: Self-nucleic acid sensing in the brain.Advances in immunology · 2024Review
- Review
- The Structural Dynamics, Complexity of Interactions, and Functions in Cancer of Multi-SAM Containing Proteins.Cancers · 2023Review
- Abnormal Intraepidermal Nerve Fiber Density in Disease: A Scoping Review.medRxiv : the preprint server for health sciences · 2023Article
- Abnormal intraepidermal nerve fiber density in disease: A scoping review.Frontiers in neurology · 2023Article
- Article
- Autophagy protein ULK1 interacts with and regulates SARM1 during axonal injury.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Sexually dimorphic effects of SARM1 deletion on cardiac NADAmerican journal of physiology. Heart and circulatory physiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Neuronal apoptosis is a key aspect of many different neurologic diseases, but the mechanisms remain unresolved. Recent studies have suggested a mechanism of innate immune-induced neuronal apoptosis through the stimulation of endosomal TLRs in neurons. TLRs are stimulated both by pathogen-associated molecular patterns as well as by damage-associated molecular patterns, including microRNAs released by damaged neurons. In the present study, we identified the mechanism responsible for TLR7/TLR9-mediated neuronal apoptosis. TLR-induced apoptosis required endosomal localization of TLRs but was independent of MyD88 signaling. Instead, apoptosis required the TLR adaptor molecule SARM1, which localized to the mitochondria following TLR activation and was associated with mitochondrial accumulation in neurites. Deficiency in SARM1 inhibited both mitochondrial accumulation in neurites and TLR-induced apoptosis. These studies identify a non-MyD88 pathway of TLR7/ TLR9 signaling in neurons and provide a mechanism for how innate immune responses in the CNS directly induce neuronal damage.
Indexed as
Identifiers
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.