ArticleMolecular neurobiology2019
Targeting Axon Integrity to Prevent Chemotherapy-Induced Peripheral Neuropathy.
Article in Molecular neurobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Microtubule Cytoskeleton Dysfunction in Chronic Pain: Mechanisms of Transport Failure and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Cancer pain.Nature reviews. Disease primers · 2026Review
- Otilonium bromide ameliorates paclitaxel-induced peripheral neuropathy by targeting phosphatase PPM1A.Journal of neuroinflammation · 2026Article
- Disproportionality Analysis of Fluoroquinolone-Associated Peripheral Neuropathy in the FAERS Database (2007-2024).Clinical and translational science · 2026Article
- Exploring Mechanistic Insights by Carotenoids in Neuropathic and Inflammatory Pain.Current neuropharmacology · 2026Review
- Microglial Deletion of Hrh4 Alleviates Alzheimer's Disease Pathologies by Enhancing Microglial Phagocytosis of Amyloid-β and Tau.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcription factor activator protein 4 (AP4)-mediated intrinsic control of axon regeneration.Science advances · 2025Article
- Acupuncture for preventing chemotherapy-induced peripheral neuropathy: study protocol for a randomised controlled trial.BMJ open · 2025Article
- Nanotechnology Approaches for Prevention and Treatment of Chemotherapy-Induced Neurotoxicity, Neuropathy, and Cardiomyopathy in Breast and Ovarian Cancer Survivors.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- Endoplasmic reticular stress as an emerging therapeutic target for chronic pain: a narrative review.British journal of anaesthesia · 2024Review
- Real-time field-programmable gate array-based closed-loop deep brain stimulation platform targeting cerebellar circuitry rescues motor deficits in a mouse model of cerebellar ataxia.CNS neuroscience & therapeutics · 2024Article
- Current understanding of the molecular mechanisms of chemotherapy-induced peripheral neuropathy.Frontiers in molecular neuroscience · 2024Review
- Protease-Activated Receptor 2 (PAR2) Expressed in Sensory Neurons Contributes to Signs of Pain and Neuropathy in Paclitaxel Treated Mice.The journal of pain · 2023Article
- Mechanistic insights into heat shock protein 27, a potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- PGC1α: an emerging therapeutic target for chemotherapy-induced peripheral neuropathy.Therapeutic advances in neurological disorders · 2023Review
- A small molecule M1 promotes optic nerve regeneration to restore target-specific neural activity and visual function.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Oral Administration of Glutathione Trisulfide Increases Reactive Sulfur Levels in Dorsal Root Ganglion and Ameliorates Paclitaxel-Induced Peripheral Neuropathy in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Cerebellar glutamatergic system impacts spontaneous motor recovery by regulating Gria1 expression.NPJ Regenerative medicine · 2022Article
- Discovery of Potential Neuroprotective Agents against Paclitaxel-Induced Peripheral Neuropathy.Journal of medicinal chemistry · 2022Article
- Endoplasmic Reticulum Stress in Chemotherapy-Induced Peripheral Neuropathy: Emerging Role of Phytochemicals.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Chemotherapy-induced peripheral neuropathy (CIPN) is an irreversible off-target adverse effect of many chemotherapeutic agents such as paclitaxel, yet its mechanism is poorly understood and no preventative measure is available. CIPN is characterized by peripheral nerve damages resulting in permanent sensory function deficits. Our recent unbiased genome-wide analysis revealed that heat shock protein (Hsp) 27 is part of a transcriptional network induced by axonal injury and highly enriched for genes involved in adaptive neuronal responses, particularly axonal regeneration. To examine if Hsp27 could prevent the occurrence of CIPN, we first demonstrated that paclitaxel-induced allodynia was associated directly with axonal degeneration in sensory neurons in a mouse model of CIPN. We therefore hypothesize that by preventing axonal degeneration could prevent the development of CIPN. We drove expression of human Hsp27 (hHsp27) specifically in neurons. Development of mechanical and thermal allodynia was prevented completely in paclitaxel-treated hHsp27 transgenic mice. Strikingly, hHsp27 protected against paclitaxel-induced neurotoxicity in vivo including degeneration of afferent nerve fibers, demyelination, mitochondrial swelling, apoptosis, and restored sensory nerve action potential. Finally, we delineated signaling cascades that link CIPN development to caspase 3 and RhoA/cofilin activation in sensory neurons and peripheral nerves. hHsp27 exerted anti-apoptotic effect and maintained axon integrity by restoring caspase 3 and RhoA expression to basal levels. Taken together, our data suggest that by preventing axonal degeneration might prove beneficial as anti-CIPN drugs, which represents an emerging research area for therapeutic development.
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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.