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Riera, Céline E., Huising, Mark O., & Follett, P. (2014). Trpv1 pain receptors regulate longevity and metabolism by neuropeptide signaling. Cell, 157(5), 1023–1036. Added by: Dr. Enrique Feoli (08/12/2023, 19:36) Last edited by: Dr. Enrique Feoli (18/08/2026, 12:13) |
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| Resource type: Journal Article Published DOI: https://doi.org/10.1016/j.cell.2014.03.051 ID no. (ISBN etc.): 0092-8674 BibTeX citation key: Riera2014 View all bibliographic details  |
Categories: BioAcyl Corp Subcategories: TPRV1 Creators: Follett, Huising, Riera Collection: Cell |
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| Abstract |
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Summary The sensation of pain is associated with increased mortality, but it is unknown whether pain perception can directly affect aging. We find that mice lacking TRPV1 pain receptors are long-lived, displaying a youthful metabolic profile at old age. Loss of TRPV1 inactivates a calcium-signaling cascade that ends in the nuclear exclusion of the CREB-regulated transcriptional coactivator CRTC1 within pain sensory neurons originating from the spinal cord. In long-lived TRPV1 knockout mice, CRTC1 nuclear exclusion decreases production of the neuropeptide CGRP from sensory endings innervating the pancreatic islets, subsequently promoting insulin secretion and metabolic health. In contrast, CGRP homeostasis is disrupted with age in wild-type mice, resulting in metabolic decline. We show that pharmacologic inactivation of CGRP receptors in old wild-type animals can restore metabolic health. These data suggest that ablation of select pain sensory receptors or the inhibition of CGRP are associated with increased metabolic health and control longevity.
• Mutation of TRPV1 extends lifespan in mice and worms via CRTC1/CREB signaling • TRPV1 mutant mice have normal growth but have a youthful metabolism late in life • TRPV1 impact on metabolism through secretion of CGRP, an insulin secretion blocker • Chemical inhibition of CGRP increases metabolic health at old age Added by: Dr. Enrique Feoli Last edited by: Dr. Enrique Feoli |
