{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T14:01:20Z","timestamp":1785333680113,"version":"3.55.0"},"reference-count":73,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T00:00:00Z","timestamp":1762732800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,11,10]],"date-time":"2025-11-10T00:00:00Z","timestamp":1762732800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The regulation of macrophage function, particularly that of monocyte\u2010derived macrophages (MoMs), by mechanical forces during myocardial infarction (MI) remains poorly understood. Consistently upregulated Piezo1 expression in cardiac macrophages and MoMs post\u2010MI is found. Elevated Piezo1 expression in MoMs directly contributes to increased Piezo1 levels in cardiac macrophages. Myeloid cell\u2010specific Piezo1\u2010deficient mice (Piezo1\n                    <jats:sup>Lyz2<\/jats:sup>\n                    ) exhibit significant improvements in ventricular function\/remodeling after MI, accompanied by decreased apoptotic cardiomyocytes and decreased inflammation, increased numbers of macrophages, and increased border zone efferocytosis. In vitro, Piezo1 activation by Yoda1 increased oxygen\u2010glucose deprivation (OGD)\u2010induced ferroptosis and impaired MoM efferocytosis. Conversely, Piezo1 deficiency in MoMs decreases ferroptosis and increases efferocytosis. SLC7A11 is shown to mediate Piezo1\u2010induced defective efferocytosis in MoMs. Piezo1 activation aggravated OGD\u2010induced macrophage ferroptosis via Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx followed by SLC15A3 upregulation. Piezo1 upregulated SLC7A11 in macrophages via a Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \/ATF4\u2010dependent pathway. MoM\u2010specific SLC7A11 knockdown significantly increases efferocytosis, reduces cardiomyocyte apoptosis and inflammation, and ameliorates post\u2010MI left ventricular remodeling and function. In conclusion, early Piezo1 activation in MoMs is identified during MI, which governs the fate and function of recruited macrophages. These data establish an ischemic heart\u2013bone marrow functional network and provide a novel therapeutic strategy in which MoM Piezo1 is targeted for post\u2013MI heart repair.\n                  <\/jats:p>","DOI":"10.1002\/advs.202510991","type":"journal-article","created":{"date-parts":[[2025,11,11]],"date-time":"2025-11-11T05:37:22Z","timestamp":1762839442000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":12,"title":["Piezo1 Upregulation in Monocyte\u2010Derived Macrophages Impairs Post\u2010Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis"],"prefix":"10.1002","volume":"13","author":[{"given":"Lu","family":"Peng","sequence":"first","affiliation":[{"name":"Department of Cardiology Xijing Hospital Fourth Military Medical University  Xi'an 710032 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