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. 2022 Jun 6;10:44. doi: 10.1038/s41413-022-00217-w

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — The interoception of bone and EP4-hypothalamus-sympathetic axis in regulating bone formation. The secretion of prostaglandin-E2 (PGE2) by osteoblasts is increased when osteoclast bone resorption occurs and bone density decreases. PGE2 binds to the prostaglandin E receptor 4 (EP4) on sensory nerve fibers, and the signals are relayed to the hypothalamus by afferent nerves. As a result, sympathetic tone is tuned down and the expression of hypothalamic neuropeptide Y (NPY) is downregulated and induces lipolysis of adipose tissue for osteoblastic bone formation.