Research ArticlePain

The stress regulator FKBP51 drives chronic pain by modulating spinal glucocorticoid signaling

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Science Translational Medicine  10 Feb 2016:
Vol. 8, Issue 325, pp. 325ra19
DOI: 10.1126/scitranslmed.aab3376

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A key to chronic pain

Our treatment tools are distressingly poor for alleviating long-lasting, debilitating pain, so new ideas are welcome. Maiarù et al. now find that inhibition of spinal cord FKBP51—a stress-related protein involved with glucocorticoid signaling—can curtail the development of chronic pain in animal models. More important for clinical application, siRNA inhibition or a newly developed FKBP51 inhibitor, SAFit2, can interrupt a preexisting chronic pain state. The authors also amass evidence from their mouse models that FKBP51 acts on chronic pain via the glucocorticoid signaling pathway. Variation in the human gene FKBP51 alters pain severity after trauma, lending confidence that drugs like SAFit2 may help patients suffering from chronic pain.

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