ArticleCNS neuroscience & therapeutics2024
DNA damage induced PARP-1 overactivation confers paclitaxel-induced neuropathic pain by regulating mitochondrial oxidative metabolism.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Olaparib Blocks Oxidative Stress-Dependent NLRP3 Inflammasome in Pediatric Acute Lung Injury by Metabolic Reprogramming via AMPK-Driven Autophagic Flux.The Kaohsiung journal of medical sciences · 2026Article
- Paclitaxel-induced germline DNA-damage signatures independent of mismatch repair inFrontiers in pharmacology · 2026Article
- Relevance and application of sirtuin 3-activated mitophagy in gastric cancer treatment.World journal of clinical oncology · 2025Review
- Peroxiredoxins in central nervous system: implications for chronic pain and anaesthetic-induced neurotoxicity management.Redox biology · 2025Review
- Review
- DNA damage induced PARP-1 overactivation confers paclitaxel-induced neuropathic pain by regulating mitochondrial oxidative metabolism.CNS neuroscience & therapeutics · 2024Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
aimsPoly (ADP-ribose) polymerase (PARP) has been extensively investigated in human cancers. Recent studies verified that current available PARP inhibitors (Olaparib or Veliparib) provided clinical palliation of clinical patients suffering from paclitaxel-induced neuropathic pain (PINP). However, the underlying mechanism of PARP overactivation in the development of PINP remains to be investigated. METHODS AND
resultsWe reported induction of DNA oxidative damage, PARP-1 overactivation, and subsequent nicotinamide adenine dinucleotide (NAD
conclusionThe findings provide a novel insight into the mechanism of DNA oxidative damage in the development of PINP and implicate PARP-1 as a possible therapeutic target for clinical PINP treatment.
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Registered trials
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