{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T18:06:03Z","timestamp":1785434763402,"version":"3.56.0"},"reference-count":32,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T00:00:00Z","timestamp":1783987200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Experimental Physiology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Despite advancements in reperfusion therapy, myocardial ischaemia\u2013reperfusion (IR) injury remains a major clinical challenge. This study investigated whether a novel dual\u2010target pre\u2010conditioning strategy using sinomenine and irisin could enhance myocardial resistance against IR injury. Ninety male Sprague\u2013Dawley rats were utilized. Protocol 1 evaluated cardioprotection by assigning rats to Sham, IR, sinomenine, irisin or a combination of both agents, with pharmacological pre\u2010treatments administered for 7\u00a0days prior to surgery. To model IR injury in vivo, animals underwent 30 min surgical ligation of the left anterior descending coronary artery followed by 24 h reperfusion. Combined pre\u2010treatment exerted superior protection, significantly reducing infarct size (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0187) and serum cardiotroponin\u2010I (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0028), while preserving myocardial architecture. Echocardiography and haemodynamic monitoring confirmed significantly enhanced ejection fraction (\n                    <jats:italic>P\u00a0<\/jats:italic>\n                    &lt;\u00a00.0001), fractional shortening (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0002), developed pressure (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0001), +d\n                    <jats:italic>P<\/jats:italic>\n                    \/d\n                    <jats:italic>t<\/jats:italic>\n                    (\n                    <jats:italic>P\u00a0<\/jats:italic>\n                    &lt;\u00a00.0001), and \u2212d\n                    <jats:italic>P<\/jats:italic>\n                    \/d\n                    <jats:italic>t<\/jats:italic>\n                    (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0003), alongside reduced left ventricular internal diameter at end\u2010systole (\n                    <jats:italic>P\u00a0<\/jats:italic>\n                    &lt;\u00a00.0001) and end\u2010diastole (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0004), as well as decreased end\u2010diastolic pressure (\n                    <jats:italic>P<\/jats:italic>\n                    \u00a0=\u00a00.0128) in the combination group. Protocol 2 investigated mechanisms using mitochondrial division inhibitor 1 (Mdivi\u20101). Combined pre\u2010treatment mitigated oxidative stress, suppressed pro\u2010inflammatory cytokines and inhibited the nucleotide\u2010binding oligomerization domain\u2010like receptor protein 3 (NLRP3) inflammasome, evidenced by significant reductions in NLRP3, apoptosis\u2010associated speck\u2010like protein containing a CARD, and cleaved Gasdermin D. Conversely, it significantly upregulated PTEN\u2010induced putative kinase 1 (PINK1) and Parkin. Notably, Mdivi\u20101 abrogated these benefits, confirming that the enhanced protection is mediated through the activation of the PINK1\/Parkin\u2010dependent mitophagy pathway. These results suggest that pharmacological pre\u2010conditioning with sinomenine and irisin offers a potent strategy against IR injury by modulating the mitophagy\u2013pyroptosis axis.\n                  <\/jats:p>","DOI":"10.1113\/ep093586","type":"journal-article","created":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T09:55:09Z","timestamp":1784022909000},"page":"3557-3569","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Therapeutic intervention with sinomenine and irisin to preserve cardiac function after ischaemia\u2013reperfusion injury"],"prefix":"10.1113","volume":"111","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-4771-4454","authenticated-orcid":false,"given":"Lianjun","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Cardiology Harbin 242 Hospital  Harbin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sining","family":"Bi","sequence":"additional","affiliation":[{"name":"Department of Cardiology Jinan Third People's Hospital  Jinan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amany","family":"Belal","sequence":"additional","affiliation":[{"name":"College of Pharmacy, Pharmaceutical Chemistry Department Taif University  Taif Saudi Arabia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-6624-4537","authenticated-orcid":false,"given":"Zhuzhu","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine Xi'an International Medical Center Hospital  Xi'an China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,7,14]]},"reference":[{"issue":"3","key":"e_1_2_9_2_1","first-page":"116","article-title":"Realizing the therapeutic potential of novel 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