ArticleCell biology and toxicology2025
Single-nucleus rna sequencing identifies universal camk1d upregulation and dysregulated c-ltmr subtypes as key drivers of paclitaxel-induced neuropathy.
Article in Cell biology and toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Single-cell and single-nucleus transcriptomics of the dorsal root ganglion in neuropathic pain: cell-state remodeling and translational prospects.Journal of translational medicine · 2026Review
- Proteomic Adaptations in the Spinal Cord of a Breast Cancer Model of Paclitaxel-Induced Peripheral Neuropathy.Journal of proteome research · 2026Article
- Using an integrated omics approach to uncover the mechanisms underlying chemotherapy-induced peripheral neuropathy (CIPN).Communications medicine · 2026Review
- The Kv4.3 channel on c-low threshold mechanoreceptors in DRG is a key mediator transforming tactile stimuli into nociceptive signals in chemotherapy-induced neuropathy.Acta pharmaceutica Sinica. B · 2026Article
- PACAP Alleviates Paclitaxel-Induced Peripheral Neuropathy by Targeting Oxidative Stress and Mitochondrial Damage via the PGC-1α Pathway.CNS neuroscience & therapeutics · 2026Article
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Authors and funding
10 authors.
Funding
Abstract
Neuropathic pain triggered by chemotherapy poses a significant clinical challenge. Investigating cell type-specific alterations through single-cell transcriptome analysis holds promise in understanding symptom development and pathogenesis. In this study, we performed single nuclei RNA (snRNA) sequencing of dorsal root ganglions (DRG) to explore the molecular mechanism underlying paclitaxel-induced neuropathic pain. Mouse exposed to repeated paclitaxel doses developed persistent pain hypersensitivity lasting at least 21 days. The snRNA sequencing unveiled seven major cell types within DRGs, with neurons further subdivided into 12 distinct subclusters using known markers. Notably, type C low-threshold mechanoreceptors (C_LTMR) exhibited the most pronounced transcriptomic changes post-paclitaxel administration. Differential gene expression and Gene Ontology (GO) analysis highlighted suppressed potassium-related currents, microtubule transport, and mitochondrial functions in C_LTMR following paclitaxel treatment. Pseudo-time analysis uncovered nine distinct states (state 1 to 9) of C_LTMR. State 1 exhibits higher prevalence in paclitaxel-treated mice and altered neurotransmission properties, likely contributing to paclitaxel-induced pain hypersensitivity. Additionally, Camk1d is involved in temperature hyperalgesia in CIPN, a key clinical symptom observed in human patients with CIPN. This comprehensive exploration sheds light on the molecular mechanisms driving paclitaxel-induced neuropathic pain, offering potential avenues for therapeutic intervention.
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