ArticleScience translational medicine2016
The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling.
Article in Science translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
The trial behind it
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Who cites it
57 citing papers in PubMed, 108 citations in OpenAlex.
- Dual proximity-based interactome mapping of FKBP51 and FKBP52 uncovers shared metabolic networks.Biochemical and biophysical research communications · 2026Article
- Targeting neuronal FKBP5 attenuates mechanical allodynia by suppressing NF-κB-mediated neuroinflammation in an NTG-induced chronic migraine mouse model.The journal of headache and pain · 2026Article
- Orofacial pain and dementia: a brief narrative review of associations, putative mechanisms, and relevant clinical considerations.Odontology · 2026Review
- FKBP51 inhibition by SAFit2 modulates tau pathology and cognitive deficits in PS19 mice.Alzheimer's research & therapy · 2026Article
- Psilocybin ameliorates neuropathic pain-like behaviour in mice and facilitates gabapentin-mediated analgesia.Communications biology · 2026Article
- Central amygdalaNeurobiology of stress · 2026Article
- Analgesia through FKBP51 inhibition at disease onset confers lasting relief from sensory and emotional chronic pain symptoms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Modeling Pain Without Injury: Inherited Rodent Models as Mechanistic Windows into Chronic Pain.Function (Oxford, England) · 2025Review
- Childhood exposure to danger increases Black youths' alcohol consumption, accelerated aging, and cardiac risk as young adults: A test of the incubation hypothesis.Development and psychopathology · 2025Article
- FKBP5 Induces Senescence in BMSCs and Inhibits Osteogenic Differentiation Through the Canonical WNT/β-Catenin Signalling Pathway in Senile Osteoporosis.Journal of cellular and molecular medicine · 2025Article
- Depletion ofInternational journal of molecular sciences · 2025Article
- Differences in multidimensional phenotype of 2 joint pain models link early weight-bearing deficit to late depressive-like behavior in male mice.Pain reports · 2024Article
- Gene expression in the dorsal root ganglion and the cerebrospinal fluid metabolome in polyneuropathy and opioid tolerance in rats.IBRO neuroscience reports · 2024Article
- Critical Windows: Exploring the Association Between Perinatal Trauma, Epigenetics, and Chronic Pain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- FKBP51-Hsp90 Interaction-Deficient Mice Exhibit Altered Endocrine Stress Response and Sex Differences Under High-Fat Diet.Molecular neurobiology · 2024Article
- Large-scale, in-cell photocrosslinking at single-residue resolution reveals the molecular basis for glucocorticoid receptor regulation by immunophilins.Nature structural & molecular biology · 2023Article
- The transcriptional regulator KLF15 is necessary for myoblast differentiation and muscle regeneration by activating FKBP5.The Journal of biological chemistry · 2023Article
- A DNA methylation signature in the stress driver gene Fkbp5 indicates a neuropathic component in chronic pain.Clinical epigenetics · 2023Article
- CpG Methylation Levels in HPA Axis Genes Predict Chronic Pain Outcomes Following Trauma Exposure.The journal of pain · 2023Article
- SAFit2 ameliorates paclitaxel-induced neuropathic pain by reducing spinal gliosis and elevating pro-resolving lipid mediators.Journal of neuroinflammation · 2023Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Polymorphisms in FKBP51 are associated with stress-related psychiatric disorders and influence the severity of pain symptoms experienced after trauma. We report that FKBP51 (FK506 binding protein 51) is crucial for the full development and maintenance of long-term pain states. Indeed, FKBP51 knockout mice, as well as mice in which silencing of FKBP51 is restricted to the spinal cord, showed reduced hypersensitivity in several persistent pain models in rodents. FKBP51 deletion did not compromise the detection of acute painful stimuli, a critical protective mechanism. Moreover, the intrathecal administration of the specific FKBP51 inhibitor SAFit2 reduced the severity of an established pain state, confirming the crucial role of spinal FKBP51 in nociceptive processing. Finally, glucocorticoid signaling, which is known to modulate persistent pain states in rodents, was impaired in FKBP51 knockout mice. This finding suggested that FKBP51 regulates chronic pain by modulation of glucocorticoid signaling. Thus, FKBP51 is a central mediator of chronic pain, likely in humans as well as rodents, and is a new pharmacologically tractable target for the treatment of long-term pain states.
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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.