{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T13:07:53Z","timestamp":1789218473846,"version":"build-2803163510"},"reference-count":45,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T00:00:00Z","timestamp":1789171200000},"content-version":"vor","delay-in-days":254,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100020595","name":"National Science and Technology Council","doi-asserted-by":"publisher","award":["NSTC 114-2314-B-039-031"],"award-info":[{"award-number":["NSTC 114-2314-B-039-031"]}],"id":[{"id":"10.13039\/100020595","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100020595","name":"National Science and Technology Council","doi-asserted-by":"publisher","award":["NSTC 114-2314-B-039-087"],"award-info":[{"award-number":["NSTC 114-2314-B-039-087"]}],"id":[{"id":"10.13039\/100020595","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010002","name":"Ministry of Education","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100010002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Pain Research and Management"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Fibromyalgia (FM) is a difficult\u2010to\u2010cure disease, and finding effective pain management methods is crucial for providing clinicians and healthcare. Adiponectin (ADP) is considered a peripheral metabolic hormone, but its role in the central nervous system remains unknown, especially in pain management. Electroacupuncture (EA) has long been scientifically proven as an effective therapy for pain relief.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We aimed to investigate the molecular mechanisms in the thalamus, somatosensory cortex, anterior cingulate cortex, and medial prefrontal cortex during intermittent cold stress (ICS)\u2013induced FM in mice, and the inhibitory effects of 2\u2010Hz EA stimulation or intracerebral ventricle (ICV) injection of ADP on this FM model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Results showed that the FM group significantly produced mechanical and thermal hyperalgesia (\n                      <jats:sup>\u2217<\/jats:sup>\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20099), while the FM\u2009+\u2009EA and FM\u2009+\u2009ADP groups showed significant reductions in mechanical and thermal hyperalgesia (\n                      <jats:sup>#<\/jats:sup>\n                      <jats:italic>p<\/jats:italic>\n                      &lt; 0.05,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u20099). The extracellular vesicles high mobility group box 1 and S100 calcium\u2010binding protein B (mediators in inflammation) were detected increased while ADP was found decreased, which can be reversed by EA but not ICV injection of ADP. Western blot analysis revealed a significant decrease in adiponectin receptor 1 (AdipoR1) and related signaling pathways after ICS\u2010induced FM hyperalgesia. However, encouragingly, in the FM\u2009+\u2009EA group, EA treatment effectively increased AdipoR1 expression. Similar results were observed in the FM\u2009+\u2009ADP group. This trend was also observed in its downstream pathways including APPL1, SIRT1, AMPK\u03b1, and PPAR\u03b1. We further found a significant increase in pain\u2010related pPI3K\u2013pAkt\u2013pmTOR and pNF\u03baB pathways in the FM group, and EA or ICV\u2010administered ADP treatment inhibited these increases.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our results confirm that 2\u2010Hz EA can treat FM pain, and its mechanism of action is through the activation of AdipoR1 and its downstream related molecular pathways.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1155\/prm\/5402246","type":"journal-article","created":{"date-parts":[[2026,9,12]],"date-time":"2026-09-12T12:53:02Z","timestamp":1789217582000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Exosomal Adiponectin Plays a Role in Electroacupuncture Analgesia by Activating the Adiponectin Receptor 1 to Inhibit 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