ArticleActa pharmaceutica Sinica. B2024
Spinal astrocyte-derived interleukin-17A promotes pain hypersensitivity in bone cancer mice.
Article in Acta pharmaceutica Sinica. B, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Bone metastasis and pain research through the dual lens of bibliometrics and bioinformatics: knowledge structure, frontiers, and core pathway analysis (2015-2024).Frontiers in medicine · 2025Pooled it
- Visualized knowledge mapping on the current research trends and emerging areas of neuroimmune modulation in the past two decades.Frontiers in immunology · 2025Pooled it
- Single-cell RNA sequencing analysis of bone cancer pain model induced by Lewis lung cancer cells in male mice.Annals of medicine · 2026Article
- Cancer-related pain: A bidirectional modulator of cancer progression.Clinical and translational medicine · 2026Review
- Loss of SHP1 in Spinal Astrocytes Triggers T-Lymphocyte Infiltration and Nociceptive Hypersensitivity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Neuroimmune Crosstalk in Psoriasis: Mechanisms and Therapeutic Implications.Inflammation · 2025Review
- Fibroblast Growth Factor 8 Suppresses Neurotoxic Astrocytes and Alleviates Neuropathic Pain via Spinal FGFR3 Signaling.Neuroscience bulletin · 2025Article
- Efficacy and safety of intrathecal human umbilical cord-derived mesenchymal stromal cell therapy for bone cancer pain: a preclinical study.Stem cell research & therapy · 2025Article
- Cancer pain: molecular mechanisms and management.Molecular biomedicine · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal microglia and astrocytes are both involved in neuropathic and inflammatory pain, which may display sexual dimorphism. Here, we demonstrate that the sustained activation of spinal astrocytes and astrocyte-derived interleukin (IL)-17A promotes the progression of mouse bone cancer pain without sex differences. Chemogenetic or pharmacological inhibition of spinal astrocytes effectively ameliorates bone cancer-induced pain-like behaviors. In contrast, chemogenetic or optogenetic activation of spinal astrocytes triggers pain hypersensitivity, implying that bone cancer-induced astrocytic activation is involved in the development of bone cancer pain. IL-17A expression predominantly in spinal astrocytes, whereas its receptor IL-17 receptor A (IL-17RA) was mainly detected in neurons expressing VGLUT2 and PAX2, and a few in astrocytes expressing GFAP. Specific knockdown of IL-17A in spinal astrocytes blocked and delayed the development of bone cancer pain. IL-17A overexpression in spinal astrocytes directly induced thermal hyperalgesia and mechanical allodynia, which could be rescued by CaMKII
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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 Socratic graph.