{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T09:40:13Z","timestamp":1792662013719,"version":"4.5.0"},"reference-count":99,"publisher":"Ovid Technologies (Wolters Kluwer Health)","license":[{"start":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T00:00:00Z","timestamp":1792627200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>\n                      Apoptotic cell clearance by macrophages, termed\n                      <jats:italic toggle=\"yes\">efferocytosis<\/jats:italic>\n                      , resolves inflammation and promotes tissue repair, whereas defective efferocytosis contributes to chronic inflammatory diseases such as atherosclerosis. Putrescine biosynthesis, driven by the rate-limiting enzyme ODC1 (ornithine decarboxylase 1), has emerged as a key efferocytosis-induced metabolic pathway that promotes inflammation resolution. However, the mechanisms regulating ODC1 during atherosclerosis remain undefined. Here, we investigated the mechanisms controlling ODC1 and putrescine biosynthesis and identified a novel integrin \u03b1v\u2013FAK (focal adhesion kinase)\u2013Rac1 (Rac family small GTPase 1)\u2013STAT3 (signal transducer and activator of transcription 3)\u2013MYC (MYC proto-oncogene) signaling axis that becomes progressively impaired during atherosclerosis.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      We performed metabolomic and cytokine profiling of human atherosclerotic plaques and assessed ODC1 expression in lesional macrophages from humans and mice. Mechanistic studies used apoptotic cell\u2013 or polystyrene bead\u2013exposed macrophages,\n                      <jats:italic toggle=\"yes\">Ldlr<\/jats:italic>\n                      <jats:sup>\u2013\/<\/jats:sup>\n                      <jats:sup>\u2013<\/jats:sup>\n                      mice with hematopoietic integrin \u03b1v deficiency fed a Western-type diet, single-nuclei RNA sequencing, and bulk RNA sequencing.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Putrescine levels negatively correlated with inflammatory mediators, and ODC1 expression in lesional macrophages declined with disease progression in humans and mice. Engulfment of apoptotic cells or polystyrene beads increased ODC1 expression through an integrin \u03b1v\u2013 and actin polymerization\u2013dependent mechanism. Hematopoietic integrin \u03b1v deficiency exacerbated lesion size and necrosis, reduced efferocytosis, and decreased fibrous cap thickness. Single-nuclei RNA sequencing showed no changes in lesional cell composition but revealed activation of inflammatory pathways specifically in integrin \u03b1v\u2013deficient macrophages. Mechanistically, phagocytosis-induced ODC1 expression relied on integrin \u03b1v\u2013mediated STAT3 activation and MYC-dependent\n                      <jats:italic toggle=\"yes\">Odc1<\/jats:italic>\n                      transcription. Bulk RNA sequencing showed that apoptotic cell\u2013exposed human macrophages lacking integrin \u03b1v upregulated atherogenic mediators and inflammatory pathways, an effect reversed by restoring putrescine levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Together, these findings uncover a previously unrecognized mechanistic link between phagocytosis and macrophage metabolism, which we identify as a case of mechanometabolism, and demonstrate how its dysregulation compromises inflammation resolution and promotes atherosclerosis.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/atvbaha.126.325444","type":"journal-article","created":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T09:00:16Z","timestamp":1792659616000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Novel Mechanometabolic Signaling Cascade Linking Efferocytosis to Inflammation Resolution"],"prefix":"10.1161","author":[{"given":"Dhananjay","family":"Kumar","sequence":"first","affiliation":[{"name":"Department of Molecular and Cellular Physiology (D.K., R.P., L.F., T.-A.G., A.Q., K.M., T.A., Y.K., K.G., B.G., L.W., C.O., C.B.P., A.W.O., O.R., A.Y.), Louisiana State University Health Sciences Center at Shreveport, LA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajan","family":"Pandit","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology (D.K., R.P., L.F., T.-A.G., A.Q., K.M., T.A., Y.K., K.G., B.G., L.W., C.O., C.B.P., A.W.O., O.R., A.Y.), Louisiana State University Health Sciences Center at Shreveport, LA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0004-1513-0251","authenticated-orcid":true,"given":"Louise","family":"Frausto","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology (D.K., R.P., L.F., T.-A.G., A.Q., K.M., T.A., Y.K., K.G., B.G., L.W., C.O., C.B.P., A.W.O., O.R., A.Y.), Louisiana State University Health Sciences Center at Shreveport, LA."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0006-5715-7123","authenticated-orcid":true,"given":"Theresea-Anne","family":"Governale","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Physiology (D.K., R.P., L.F., T.-A.G., A.Q., K.M., T.A., Y.K., K.G., B.G., L.W., C.O., C.B.P., A.W.O., O.R., A.Y.), Louisiana State University Health Sciences Center at Shreveport, 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