ArticleCancer chemotherapy and pharmacology2014
Toll-like receptor signaling regulates cisplatin-induced mechanical allodynia in mice.
Article in Cancer chemotherapy and pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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
43 citing papers in PubMed, 65 citations in OpenAlex.
- Pharmacological Inhibition of JAK/STAT-IL2 Axis Alleviated Cisplatin-Induced Ototoxicity.Molecular neurobiology · 2025Article
- Chronic treatment with carboplatin induces mechanical hypersensitivity and neurochemical changes in the mouse dorsal root ganglia and spinal cord.Cancer chemotherapy and pharmacology · 2025Article
- Myeloid Differentiation Primary Response Protein 88: An Important Therapeutic Target for Chronic Pain.Journal of pain research · 2025Review
- TLR-4: a promising target for chemotherapy-induced peripheral neuropathy.Molecular biology reports · 2024Review
- Targeting therapy-induced senescence as a novel strategy to combat chemotherapy-induced peripheral neuropathy.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2024Review
- Mesenchymal stem cell transplantation plays a role in relieving cancer pain.Frontiers in pharmacology · 2024Review
- PNA6, a Lactosyl Analogue of Angiotensin-(1-7), Reverses Pain Induced in Murine Models of Inflammation, Chemotherapy-Induced Peripheral Neuropathy, and Metastatic Bone Disease.International journal of molecular sciences · 2023Article
- Milnacipran Has an Antihyperalgesic Effect on Cisplatin-Induced Neuropathy.Pharmaceutics · 2023Article
- Kinin BPharmaceuticals (Basel, Switzerland) · 2023Article
- Kinin BPharmaceutics · 2023Article
- Toll-like Receptors and Thrombopoiesis.International journal of molecular sciences · 2023Review
- Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022Review
- Review
- Role of innate immunity in chemotherapy-induced peripheral neuropathy.Neuroscience letters · 2021Review
- Review
- Review
- Article
- Peripheral Neuropathy under Oncologic Therapies: A Literature Review on Pathogenetic Mechanisms.International journal of molecular sciences · 2021Review
- Review of the Role of the Brain in Chemotherapy-Induced Peripheral Neuropathy.Frontiers in molecular biosciences · 2021Review
- Gut microbiota regulates neuropathic pain: potential mechanisms and therapeutic strategy.The journal of headache and pain · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
purposeCisplatin-treated mice develop a persistent pain state and a condition wherein otherwise innocuous tactile stimuli evoke pain behavior, e.g., tactile allodynia. The allodynia is associated with an up-regulation of activation transcription factor 3 (ATF3) in the dorsal root ganglia (DRG), a factor, which is activated by Toll-like receptors (TLRs). Accordingly, we sought to examine the role of the TLR signaling cascade on allodynia, weight, and changes in DRG ATF3 in cisplatin-treated mice.
methodsCisplatin (2.3 mg/kg/day × 6 injections every other day) or vehicle was administered to male wild-type (WT) C57BL/6, Tlr3 (-/-), Tlr4 (-/-), Myd88 (-/-), Trif (lps2) and Myd88/Trif (lps2) mice. We examined allodynia and body weight at intervals over 30 days, when we measured DRG ATF3 by immunostaining.
results(1) WT cisplatin-treated mice showed tactile allodynia from day 3 through day 30. (2) The Myd88/Trif (lps2) mice did not show allodynia. (3) In Tlr3 (-/-), Tlr4 (-/-), and Myd88 (-/-) mice, withdrawal thresholds were elevated toward normal versus WT cisplatin-treated mice, but remained decreased as compared to vehicle mice. (4) In Trif (lps2) mice, cisplatin allodynia showed a delayed onset, but persisted. (5) In Tlr3 (-/-), Tlr4 (-/-), Myd88 (-/-), and Myd88/Trif (lps2) mice, the increase in DRG ATF3 was abolished. (6) Weight loss occurred during cisplatin administration, which was exacerbated in mutant as compared to WT mice.
conclusionsCisplatin evoked a persistent allodynia and DRG ATF3 expression in WT mice, but these effects were reduced in mice with TLR signaling deficiency. TLR signaling may thus be involved in the mechanisms leading to the cisplatin polyneuropathy.
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.