ArticlePain2019
Repressor element 1-silencing transcription factor drives the development of chronic pain states.
Article in Pain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Temporal Transcriptomic Changes in the Cingulate Cortex of Neuropathic Pain Mice.Biomedicines · 2026Article
- 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
- Transcriptomic signatures of the insular cortex in a mouse model of neuropathic pain.Frontiers in molecular neuroscience · 2026Article
- Peroxisome, neuropeptide, and inflammation signaling pathways uniquely impacted by opioid exposure in the hypothalamus of males and females.Molecular and cellular neurosciences · 2025Article
- The intersection of endocrine signaling and neuroimmune communication regulates muscle inflammation-induced nociception in neonatal mice.Brain, behavior, and immunity · 2025Article
- The effect of ponicidin on CFA-induced chronic inflammatory pain and its mechanism based on network pharmacology and molecular docking.Frontiers in medicine · 2025Article
- Involvement of sphingosine-1-phosphate receptor 1 in pain insensitivity in a BTBR mouse model of autism spectrum disorder.BMC medicine · 2024Article
- Article
- Selective KCNQ2/3 Potassium Channel Opener ICA-069673 Inhibits Excitability in Mouse Vagal Sensory Neurons.The Journal of pharmacology and experimental therapeutics · 2024Article
- REST Is Not Resting: REST/NRSF in Health and Disease.Biomolecules · 2023Review
- A compendium of validated pain genes.WIREs mechanisms of disease · 2022Review
- Age‑related differences for expression of the nerve‑specific proteins after peripheral nerve injury.Experimental and therapeutic medicine · 2022Article
- Repressor element 1-silencing transcription factor deficiency yields profound hearing loss through KeLife · 2022Article
- The functions of repressor element 1-silencing transcription factor in models of epileptogenesis and post-ischemia.Metabolic brain disease · 2021Review
- C-terminal domain small phosphatase 1 (CTDSP1) regulates growth factor expression and axonal regeneration in peripheral nerve tissue.Scientific reports · 2021Article
- Epigenetics Involvement in Oxaliplatin-Induced Potassium Channel Transcriptional Downregulation and Hypersensitivity.Molecular neurobiology · 2021Article
- Peripheral Voltage-Gated Cation Channels in Neuropathic Pain and Their Potential as Therapeutic Targets.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Antinociceptive effect of intrathecal injection of miR-9-5p modified mouse bone marrow mesenchymal stem cells on a mouse model of bone cancer pain.Journal of neuroinflammation · 2020Article
- Inhibition of M/KFrontiers in molecular neuroscience · 2020Article
- Sex differences in nerve injury-induced neuropathic pain via REST in primary sensory neurons.Neurobiology of pain (Cambridge, Mass.)Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Chronic pain is an unmet clinical problem with vast individual, societal, and economic impact. Pathologic activity of the peripheral somatosensory afferents is one of the major drivers of chronic pain. This overexcitable state of somatosensory neurons is, in part, produced by the dysregulation of genes controlling neuronal excitability. Despite intense research, a unifying theory behind neuropathic remodelling is lacking. Here, we show that transcriptional suppressor, repressor element 1-silencing transcription factor (REST; neuron-restrictive silencing factor, NRSF), is necessary and sufficient for the development of hyperalgesic state after chronic nerve injury or inflammation. Viral overexpression of REST in mouse dorsal root ganglion (DRG) induced prominent mechanical and thermal hyperalgesia in vivo. Sensory neuron-specific, inducible Rest knockout prevented the development of such hyperalgesic state in 3 different chronic pain models. Genetic deletion of Rest reverted injury-induced hyperalgesia. Moreover, viral overexpression of REST in the same neurons in which its gene has been genetically deleted restored neuropathic hyperalgesia. Finally, sensory neuron specific Rest knockout prevented injury-induced downregulation of REST target genes in DRG neurons. This work identified REST as a major regulator of peripheral somatosensory neuron remodelling leading to chronic pain. The findings might help to develop a novel therapeutic approache to combat chronic pain.
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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.