{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T12:56:43Z","timestamp":1792587403682,"version":"4.5.0"},"reference-count":40,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2024,5,16]],"date-time":"2024-05-16T00:00:00Z","timestamp":1715817600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Acta Physiologica"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aim<\/jats:title>\n                    <jats:p>To reveal the contribution of Irisin in the beneficial effects of resistance exercise on myocardial fibrosis (MF) and cardiac function in the mice with myocardial infarction (MI).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The MI model was built by ligating the left anterior descending coronary artery in\n                      <jats:italic>Fndc5<\/jats:italic>\n                      knockout mice (\n                      <jats:italic>Fndc5<\/jats:italic>\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ). Resistance exercise was started one week after surgery and continued for four weeks. In addition, H\n                      <jats:sub>2<\/jats:sub>\n                      O\n                      <jats:sub>2<\/jats:sub>\n                      , AICAR, recombinant human Irisin protein (rhIRISIN), and Sirt1 shRNA lentivirus (LV\u2010\n                      <jats:italic>Sirt1<\/jats:italic>\n                      shRNA) were used to intervene primary isolated cardiac fibroblasts (CFs). MF was observed through Masson staining, and apoptosis was assessed using TUNEL staining. MDA and T\u2010SOD contents were detected by biochemical kits. The expression of proteins and genes was detected by Western blotting and RT\u2010qPCR.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Resistance exercise increased\n                      <jats:italic>Fndc5<\/jats:italic>\n                      mRNA level, inhibited the activation of TGF\u03b21\u2010TGF\u03b2R2\u2010Smad2\/3 pathway, activated AMPK\u2010Sirt1 pathway, reduced the levels of oxidative stress, apoptosis, and MF in the infarcted heart, and promoted cardiac function. However,\n                      <jats:italic>Fndc5<\/jats:italic>\n                      knockout attenuated the protective effects of resistance exercise on the MI heart. Results of the\n                      <jats:italic>in vitro<\/jats:italic>\n                      experiments showed that AICAR and rhIRISIN intervention activated the AMPK\u2010Sirt1 pathway and inactivated the TGF\u03b21\u2010Smad2\/3 pathway, and promoted apoptosis in H\n                      <jats:sub>2<\/jats:sub>\n                      O\n                      <jats:sub>2<\/jats:sub>\n                      \u2010treated CFs. Notably, these effects of rhIRISIN intervention, except for the TGF\u03b2R2 expression, were attenuated by LV\u2010\n                      <jats:italic>Sirt1<\/jats:italic>\n                      shRNA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Resistance exercise upregulates\n                      <jats:italic>Fndc5<\/jats:italic>\n                      expression, activates AMPK\u2010Sirt1 pathway, inhibits the activation of TGF\u03b21\u2010Smad2\/3 pathway, attenuates MF, and promotes cardiac function after MI.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.14163","type":"journal-article","created":{"date-parts":[[2024,5,16]],"date-time":"2024-05-16T07:54:33Z","timestamp":1715846073000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Resistance exercise upregulates\n                    <scp>Irisin<\/scp>\n                    expression and suppresses myocardial fibrosis following myocardial infarction via activating\n                    <scp>AMPK\u2010Sirt1<\/scp>\n                    and inactivating\n                    <scp>TGF\u03b21\u2010Smad2\/3<\/scp>"],"prefix":"10.1111","volume":"240","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5770-0812","authenticated-orcid":false,"given":"Hangzhuo","family":"Li","sequence":"first","affiliation":[{"name":"Institute of Sports and Exercise Biology, School of Physical Education Shaanxi Normal University  Xi'an China"},{"name":"The Key Laboratory of Biomedical Information Engineering 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