{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T07:02:47Z","timestamp":1779692567046,"version":"3.53.1"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,25]],"date-time":"2026-05-25T00:00:00Z","timestamp":1779667200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82270998, 82571125"],"award-info":[{"award-number":["82270998, 82571125"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Osteoporosis is a systemic metabolic disease characterized by disrupted homeostasis between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Accumulating evidence indicates that chronic systemic pathological states can exert sustained effects on osteo-immune homeostasis. However, how these disturbances promote immune-mediated osteoclast dysregulation remains unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Candidate miRNAs targeting\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      were identified using bioinformatic prediction tools, and the direct interaction between miR-1a-3p and\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      was validated by dual-luciferase reporter assay. RAW264.7 cells were transfected with miR-1a-3p mimics or inhibitors to assess the effects of miR-1a-3p on osteoclast, which was evaluated by tartrate-resistant acid phosphatase (TRAP) staining, RT-qPCR, and Western blotting. miR-1a-3p expression was further analyzed in human osteoporosis cohorts and animal models of bone loss. Furthermore, to investigate whether systemic psychological stress\u2014a chronic pathological state with sustained immunoregulatory consequences\u2014regulates this axis, a chronic unpredictable mild stress (CUMS) model was established to examine stress-associated regulation of this axis. miR-1a-3p expression were detected by qRT-PCR, and Fc\u03b3RIV\u2013SYK\u2013NFATc1 pathway activation was assessed by immunofluorescence staining, qRT-PCR, and Western blot.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      as a direct target of miR-1a-3p and found that miR-1a-3p overexpression significantly suppressed osteoclast activity by inhibiting\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      -dependent signaling. Consistent with this regulatory relationship, miR-1a-3p expression was significantly reduced in both human osteoporosis cohorts and animal models of bone loss. In the CUMS model, decreased miR-1a-3p expression was accompanied by increased\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      expression, activation of the Fc\u03b3RIV\u2013SYK\u2013NFATc1 signaling pathway, enhanced osteoclast activity, and osteoporotic bone loss.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      These findings support a role for the miR-1a-3p\u2013\n                      <jats:italic>Fcgr4<\/jats:italic>\n                      axis in linking systemic pathological changes to immune-mediated osteoclast dysregulation, providing a mechanistic framework for pathological bone loss and a basis for understanding immune-bone interactions in chronic systemic diseases.\n                    <\/jats:p>\n                  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