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Purinergic signaling (adenosine, AMP, and ATP) plays a crucial role in inflammation, myogenesis, and muscle hypertrophy. Dipyridamole, an antiplatelet agent, enhances extracellular adenosine availability, alters AMP\/ATP ratio, and activates A2BR and AMP kinase (AMPK) pathways. We aim to investigate its potential use as a therapeutic agent for RA and rheumatoid sarcopenia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>K\/BxN\u2010induced mice received preventive or therapeutic dipyridamole treatment daily and were sacrificed at joint inflammation peak and resolution stage. Motor activity tests and dual\u2010energy x\u2010ray absorptiometry were performed. C\u2010reactive protein levels were also analyzed in serum, and cytokines array was performed in serum and muscle. Histology of tibialis anterior and talus joint were studied. Myogenesis, purinergic system, atrophy, and senescence key markers were analyzed via Western blot and reverse transcriptase\u2013polymerase chain reaction in gastrocnemius. Nucleotide content via high\u2010performance liquid chromatography was performed. Two\u2010dimensional and three\u2010dimensional models with C2C12 cells were done.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Dipyridamole reduced joint, muscle, and systemic inflammation, counteracting muscle wasting and physical inactivity via an anabolic mechanism involving down\u2010regulation of myostatin expression. This effect was mediated by increased adenosine and AMP levels, which activate adenosine A2BR and downstream cAMP\/AMPK signaling pathways.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results support a dual role for dipyridamole in RA, combining robust anti\u2010inflammatory effects with a novel, myostatin\u2010linked anabolic action on sarcopenia, mediated through adenosine and AMPK signaling, distinct from conventional therapeutic mechanisms.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art70047-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.70047","type":"journal-article","created":{"date-parts":[[2025,12,30]],"date-time":"2025-12-30T07:59:07Z","timestamp":1767081547000},"page":"1535-1553","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Dual Action of Dipyridamole in Experimental Rheumatoid Arthritis: Suppression of Joint Inflammation and Upregulation of Muscle Anabolism via Adenosine and\n                    <scp>AMPK<\/scp>\n                    Pathways"],"prefix":"10.1002","volume":"78","author":[{"given":"Miguel","family":"Marco\u2010Bonilla","sequence":"first","affiliation":[{"name":"Joint and Bone Research Unit, Fundaci\u00f3n Instituto de Investigaci\u00f3n Sanitaria de la Fundaci\u00f3n Jim\u00e9nez D\u00edaz Universidad Aut\u00f3noma de Madrid  Madrid 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