ReviewFrontiers in cellular neuroscience2020
Revisiting PNS Plasticity: How Uninjured Sensory Afferents Promote Neuropathic Pain.
Review in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Human pain transcriptomics: lessons learned so far.Pain reports · 2026Review
- Short-term symptom aggravation after cubital tunnel decompression: Clinical features and mechanistic insights from a retrospective cohort study.Neurosurgical review · 2026Article
- CXCL9 and CXCL10 Induce Expression of Nociceptive Ion Channels in Primary Sensory Neurons in Models of HIV-Associated Distal Sensory Polyneuropathy.International journal of molecular sciences · 2026Article
- Selection of sciatic nerve injury models: implications for pathogenesis and treatment.Frontiers in neurology · 2025Review
- The course of mechanical allodynia differs between forelimb innervation territories following median nerve injury in the rat.Frontiers in neuroscience · 2025Article
- The Intrinsic Neuronal Activation of the CXCR4 Signaling Axis Is Associated with a Pro-Regenerative State in Cervical Primary Sensory Neurons Conditioned by a Sciatic Nerve Lesion.International journal of molecular sciences · 2024Article
- Satellite Glial Cells Bridge Sensory Neuron Crosstalk in Visceral Pain and Cross-Organ Sensitization.The Journal of pharmacology and experimental therapeutics · 2024Review
- Beyond the Pain Management Clinic: The Role of AI-Integrated Remote Patient Monitoring in Chronic Disease Management - A Narrative Review.Journal of pain research · 2024Review
- Neuroinflammation in the Dorsal Root Ganglia and Dorsal Horn Contributes to Persistence of Nociceptor Sensitization in SIV-Infected Antiretroviral Therapy-Treated Macaques.The American journal of pathology · 2023Article
- An induced pluripotent stem cell-based model identifies molecular targets of vincristine neurotoxicity.Disease models & mechanisms · 2022Article
- scRNA-sequencing reveals subtype-specific transcriptomic perturbations in DRG neurons ofeLife · 2022Article
- Neuropathic ocular surface pain: Emerging drug targets and therapeutic implications.Expert opinion on therapeutic targets · 2022Review
- Neurodynamic Treatment Promotes Mechanical Pain Modulation in Sensory Neurons and Nerve Regeneration in Rats.Biomedicines · 2022Article
- Targeted ubiquitination of sensory neuron calcium channels reduces the development of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Despite the widespread study of how injured nerves contribute to chronic pain, there are still major gaps in our understanding of pain mechanisms. This is particularly true of pain resulting from nerve injury, or neuropathic pain, wherein tactile or thermal stimuli cause painful responses that are particularly difficult to treat with existing therapies. Curiously, this stimulus-driven pain relies upon intact, uninjured sensory neurons that transmit the signals that are ultimately sensed as painful. Studies that interrogate uninjured neurons in search of cell-specific mechanisms have shown that nerve injury alters intact, uninjured neurons resulting in an activity that drives stimulus-evoked pain. This review of neuropathic pain mechanisms summarizes cell-type-specific pathology of uninjured sensory neurons and the sensory ganglia that house their cell bodies. Uninjured neurons have demonstrated a wide range of molecular and neurophysiologic changes, many of which are distinct from those detected in injured neurons. These intriguing findings include expression of pain-associated molecules, neurophysiological changes that underlie increased excitability, and evidence that intercellular signaling within sensory ganglia alters uninjured neurons. In addition to well-supported findings, this review also discusses potential mechanisms that remain poorly understood in the context of nerve injury. This review highlights key questions that will advance our understanding of the plasticity of sensory neuron subpopulations and clarify the role of uninjured neurons in developing anti-pain therapies.
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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.