ArticleNeurobiology of pain (Cambridge, Mass.)
AMPK activation regulates P-body dynamics in mouse sensory neurons
Article in Neurobiology of pain (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 20 citations in OpenAlex.
- SHED-derived exosomes attenuate trigeminal neuralgia after CCI of the infraorbital nerve in mice via the miR-24-3p/IL-1R1/p-p38 MAPK pathway.Journal of nanobiotechnology · 2023Article
- Roles of AMPK and Its Downstream Signals in Pain Regulation.Life (Basel, Switzerland) · 2021Review
- Research Progress on Alzheimer's Disease and Resveratrol.Neurochemical research · 2020Review
- Metformin: A Prospective Alternative for the Treatment of Chronic Pain.Frontiers in pharmacology · 2020Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Increased mRNA translation in sensory neurons following peripheral nerve injury contributes to the induction and maintenance of chronic neuropathic pain. Metformin, a common anti-diabetic drug and an activator of AMP-activated protein kinase (AMPK), inhibits cap-dependent mRNA translation and reverses mechanical hypersensitivity caused by a neuropathic injury in both mice and rats. P-bodies are RNA granules that comprise sites for metabolizing mRNA through the process of de-capping followed by RNA decay. These RNA granules may also sequester mRNAs for storage. We have previously demonstrated that induction of cap-dependent translation in cultured trigeminal ganglion (TG) neurons decreases P-body formation and AMPK activators increase P-body formation. Here we examined the impact of AMPK activation on protein synthesis and P-body formation
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