ReviewNature reviews. Disease primers2022
Genetic pain loss disorders.
Review in Nature reviews. Disease primers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 52 citations in OpenAlex.
- Ultralow-voltage electrochemical organic light-emitting transistors with pinned and wide lateral recombination.Nature materials · 2026Article
- Functional characterization of human iPSC-derived sensory neuron processes in microfluidic cultures.Stem cells translational medicine · 2026Article
- Article
- Suspected hereditary sensory and autonomic neuropathies: clinical signs and electrodiagnostic findings in eleven dogs.Journal of veterinary internal medicine · 2026Article
- Natural antisense transcript Nat9a suppresses Scn9a (NaScientific reports · 2026Article
- Neurotrophic keratopathy in childhood: advances in understanding of pathogenesis and management.Eye (London, England) · 2026Review
- Efficient genetic perturbation of murine sensory neurons in vivo using CRISPR/Cas9.The journal of pain · 2026Article
- Mitochondrial energetic failure underlies FLVCR1-related sensory neuropathy.Communications biology · 2026Article
- Exceptionally selective voltage-sensor trapping of NaScientific reports · 2026Article
- Charcot-Marie-Tooth disease and related neuropathies.Nature reviews. Disease primers · 2026Review
- Fast-conducting mechanonociceptors uniquely engage reflexive and affective pain circuitry to drive protective responses.bioRxiv : the preprint server for biology · 2025Article
- Clinical Efficacy and Safety Profile of Suzetrigine: A Novel Non-opioid Analgesic Targeting NaV1.8 Sodium Channel.Cureus · 2025Review
- Efficient genetic perturbation of murine sensory neuronsbioRxiv : the preprint server for biology · 2025Article
- A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies.bioRxiv : the preprint server for biology · 2025Article
- Neurophysiology of acute and chronic pain: from genes to pain symptoms.BJA education · 2025Review
- Sensory neuron-expressed FGF13 controls nociceptive signaling in diabetic neuropathy models.The Journal of clinical investigation · 2025Article
- Small molecule-mediated targeted protein degradation of voltage-gated sodium channels involved in pain.bioRxiv : the preprint server for biology · 2025Article
- The genetics of pain.BJA education · 2024Review
- Article
- Broadening the Genetic Spectrum of Painful Small-Fiber Neuropathy through Whole-Exome Study in Early-Onset Cases.International journal of molecular sciences · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors at 12 institutions in 8 countries.
Funding
Abstract
Genetic pain loss includes congenital insensitivity to pain (CIP), hereditary sensory neuropathies and, if autonomic nerves are involved, hereditary sensory and autonomic neuropathy (HSAN). This heterogeneous group of disorders highlights the essential role of nociception in protecting against tissue damage. Patients with genetic pain loss have recurrent injuries, burns and poorly healing wounds as disease hallmarks. CIP and HSAN are caused by pathogenic genetic variants in >20 genes that lead to developmental defects, neurodegeneration or altered neuronal excitability of peripheral damage-sensing neurons. These genetic variants lead to hyperactivity of sodium channels, disturbed haem metabolism, altered clathrin-mediated transport and impaired gene regulatory mechanisms affecting epigenetic marks, long non-coding RNAs and repetitive elements. Therapies for pain loss disorders are mainly symptomatic but the first targeted therapies are being tested. Conversely, chronic pain remains one of the greatest unresolved medical challenges, and the genes and mechanisms associated with pain loss offer new targets for analgesics. Given the progress that has been made, the coming years are promising both in terms of targeted treatments for pain loss disorders and the development of innovative pain medicines based on knowledge of these genetic diseases.
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.