ArticleJCI insight2019
Vincristine and bortezomib use distinct upstream mechanisms to activate a common SARM1-dependent axon degeneration program.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.
What it found
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The trial behind it
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Who cites it
92 citing papers in PubMed, 149 citations in OpenAlex.
- Neurofilament light chain levels indicate acute axonal damage under bortezomib treatment.Journal of neurology · 2023Trial
- Preclinical Pharmacokinetic and Pharmacological Profiling of B339, a Novel SARM1 Inhibitor for the Treatment of Vincristine-induced Peripheral Neuropathy.Pharmaceutical research · 2026Article
- Preclinical Pharmacokinetic and Pharmacological Profiling of B339, a Novel SARM1 Inhibitor for the Treatment of Vincristine-induced Peripheral Neuropathy.Pharmaceutical research · 2026Article
- Nicotinamide Mononucleotide Adenylyltransferase 1 and NADMetabolites · 2026Review
- Chemotherapy-Induced Neurotoxicity: Molecular Mechanisms, Biomarkers and Emerging Neuroprotective Strategies.Biomedicines · 2026Review
- Human iPSC-Derived Dorsal Root Ganglion Organoid Modeling of Chemotherapy-Induced Peripheral Neuropathy.Cells · 2026Article
- SARM1 activation promotes axonal degeneration via a two-step phase transition.Nature chemical biology · 2026Article
- 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
- Combinatorial chemistry identifies additional compounds that selectively inhibit DLK-dependent retrograde signaling while minimally affecting other axonal roles of DLK.Scientific reports · 2026Article
- Programmed axon degeneration: mechanism, inhibition and therapeutic potential.Nature reviews. Neuroscience · 2026Review
- Mechanisms and treatment of cancer therapy-induced peripheral and central neurotoxicity.Nature reviews. Cancer · 2025Review
- Targeting sex-specific DRG inflammation and neurofibrosis to prevent Bortezomib-induced neuropathy.Brain, behavior, and immunity · 2025Article
- Preventing neuropathy and improving anticancer chemotherapy with a carbazole-based compound.Science advances · 2025Article
- Genetic Deletion of Sarm1 in Mouse Models of Three Neurological Diseases.Journal of the peripheral nervous system : JPNS · 2025Article
- SARM1 Inhibition in Three Mouse Models of Charcot-Marie-Tooth Disease.Journal of the peripheral nervous system : JPNS · 2025Article
- Carnosol, a Rosemary Ingredient Discovered in a Screen for Inhibitors of SARM1-NADAntioxidants (Basel, Switzerland) · 2025Article
- Recent Advances in Diagnosis, Management, Treatment, and Prevention of Neuropathies in Cancer Patients.Current neurology and neuroscience reports · 2025Review
- Design, synthesis and bioactivity evaluation of novel monomethyl auristatin F analogues.Molecular diversity · 2025Article
- Macrophage depletion restores the DRG microenvironment and prevents axon degeneration in bortezomib-induced neuropathy.bioRxiv : the preprint server for biology · 2025Article
- Bortezomib-induced peripheral neuropathy: from molecular mechanisms to clinical management.Frontiers in pharmacology · 2025Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Chemotherapy-induced peripheral neuropathy is one of the most prevalent dose-limiting toxicities of anticancer therapy. Development of effective therapies to prevent chemotherapy-induced neuropathies could be enabled by a mechanistic understanding of axonal breakdown following exposure to neuropathy-causing agents. Here, we reveal the molecular mechanisms underlying axon degeneration induced by 2 widely used chemotherapeutic agents with distinct mechanisms of action: vincristine and bortezomib. We showed previously that genetic deletion of SARM1 blocks vincristine-induced neuropathy and demonstrate here that it also prevents axon destruction following administration of bortezomib in vitro and in vivo. Using cultured neurons, we found that vincristine and bortezomib converge on a core axon degeneration program consisting of nicotinamide mononucleotide NMNAT2, SARM1, and loss of NAD+ but engage different upstream mechanisms that closely resemble Wallerian degeneration after vincristine and apoptosis after bortezomib. We could inhibit the final common axon destruction pathway by preserving axonal NAD+ levels or expressing a candidate gene therapeutic that inhibits SARM1 in vitro. We suggest that these approaches may lead to therapies for vincristine- and bortezomib-induced neuropathies and possibly other forms of peripheral neuropathy.
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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.