ArticleThe Journal of cell biology2022
Sarm1 activation produces cADPR to increase intra-axonal Ca++ and promote axon degeneration in PIPN.
Article in The Journal of cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 86 citations in OpenAlex.
- [Huangqi Guizhi Wuwu Decoction in the Treatment of Pemetrexed Intrathecal Chemotherapy-induced Neurotoxicity in NSCLC Patients with Leptomeningeal Metastases: A Randomized Controlled Trial].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2026Trial
- Loss of SARM1 Improves Phenotypes in a Mouse Model of Autosomal Recessive Spastic Ataxia of Charlevoix-Saguenay.Neurology. Genetics · 2026Article
- Aging-Related Changes in the Injury Response of the Peripheral Nervous System.Neuroscience bulletin · 2026Review
- Targeting the SARM1-cADPR-CaArthritis research & therapy · 2026Article
- The rise and fall of SARM1 base-exchange inhibitors.Communications chemistry · 2026Article
- A human iPSC-derived sensory neuron platform for high-throughput discovery of neuroprotectants against chemotherapy-induced peripheral neuropathy.Cell reports. Medicine · 2026Article
- Otilonium bromide ameliorates paclitaxel-induced peripheral neuropathy by targeting phosphatase PPM1A.Journal of neuroinflammation · 2026Article
- NADFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Molecular mechanisms of plant NLR activation and signalling.The Plant journal : for cell and molecular biology · 2026Review
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Molecular characterisation of the Bacillus subtilis SpbK antiphage defence system.Nature communications · 2025Article
- A CRISPR activation screen reveals a cilia disassembly pathway mutated in focal cortical dysplasia.Science advances · 2025Article
- Satellite glial contact enhances differentiation and maturation of human iPSC-derived sensory neurons.Stem cell reports · 2025Article
- A sensory and motor neuropathy caused by a genetic variant ofScience advances · 2025Article
- Pyruvate kinase deficiency links metabolic perturbations to neurodegeneration and axonal protection.Molecular metabolism · 2025Article
- Engineering the Future of Restorative Clinical Peripheral Nerve Surgery.Advanced healthcare materials · 2025Review
- SARM1: The Checkpoint of Axonal Degeneration in the Nervous System Disorders.Molecular neurobiology · 2025Review
- SARM1 base-exchange inhibitors induce SARM1 activation and neurodegeneration at low doses.npj drug discovery · 2025Article
- Evolutionarily ancient functions of enzymatic TIR proteins in innate immunity.Trends in immunology · 2025Review
- Targeting SARM1 as a novel neuroprotective therapy in neurotropic viral infections.Journal of neuroinflammation · 2025Article
Corrections and comments
- Commented on by
Authors and funding
15 authors at 6 institutions in 3 countries.
Funding
Abstract
Cancer patients frequently develop chemotherapy-induced peripheral neuropathy (CIPN), a painful and long-lasting disorder with profound somatosensory deficits. There are no effective therapies to prevent or treat this disorder. Pathologically, CIPN is characterized by a "dying-back" axonopathy that begins at intra-epidermal nerve terminals of sensory neurons and progresses in a retrograde fashion. Calcium dysregulation constitutes a critical event in CIPN, but it is not known how chemotherapies such as paclitaxel alter intra-axonal calcium and cause degeneration. Here, we demonstrate that paclitaxel triggers Sarm1-dependent cADPR production in distal axons, promoting intra-axonal calcium flux from both intracellular and extracellular calcium stores. Genetic or pharmacologic antagonists of cADPR signaling prevent paclitaxel-induced axon degeneration and allodynia symptoms, without mitigating the anti-neoplastic efficacy of paclitaxel. Our data demonstrate that cADPR is a calcium-modulating factor that promotes paclitaxel-induced axon degeneration and suggest that targeting cADPR signaling provides a potential therapeutic approach for treating paclitaxel-induced peripheral neuropathy (PIPN).
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.