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MAP kinase\u2010activated protein kinase 2 (MK2) regulates the stability of several pro\u2010inflammatory cytokines. Hence, this study was to determine if MK2 deficiency impaired the inflammatory phase of post\u2010MI wound repair. Myocardial infarctions were induced by permanent ligation of the left anterior descending coronary artery in 12\u2010week\u2010old male MK2<jats:sup>+\/+<\/jats:sup> and MK2<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Five days post\u2010MI, survival was 100% in MI\u2010MK2<jats:sup>\u2212\/\u2212<\/jats:sup> (<jats:italic>n<\/jats:italic>\u2009=\u200920) and 79% in MI\u2010MK2<jats:sup>+\/+<\/jats:sup> mice (<jats:italic>n<\/jats:italic>\u2009=\u200929; Mandel\u2010Cox test: <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05). Systolic and diastolic LV diameters were greater in MI\u2010MK2<jats:sup>+\/+<\/jats:sup> than MI\u2010MK2<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Infiltration of neutrophils or monocytes did not differ significantly. Cytokine and chemokine transcripts were quantified in infarcted and non\u2010infarcted LV tissue using qPCR arrays. Three days post\u2010MI, <jats:italic>Ifna2<\/jats:italic> was increased and <jats:italic>Il16<\/jats:italic> was decreased in infarcted tissue from MK2<jats:sup>\u2212\/\u2212<\/jats:sup> hearts, compared with infarcted MK2<jats:sup>+\/+<\/jats:sup> tissue, whereas in the non\u2010infarcted MK2<jats:sup>\u2212\/\u2212<\/jats:sup> myocardium <jats:italic>Il27<\/jats:italic> increased and <jats:italic>Tnfsf11<\/jats:italic>, <jats:italic>Ccl3<\/jats:italic>, and <jats:italic>Il1rn<\/jats:italic> were decreased. Five days post\u2010MI, <jats:italic>Ctf16<\/jats:italic> and <jats:italic>Il10<\/jats:italic> increased in infarcted MK2<jats:sup>\u2212\/\u2212<\/jats:sup> tissue whereas in the non\u2010infarcted MK2<jats:sup>\u2212\/\u2212<\/jats:sup> myocardium <jats:italic>Ccl9<\/jats:italic>, <jats:italic>Nodal<\/jats:italic>, and <jats:italic>Xcl2<\/jats:italic> increased and <jats:italic>Il15<\/jats:italic> decreased. These findings suggest MK2 deficiency is an advantage during the inflammatory phase of cardiac wound repair post\u2010MI.<\/jats:p>","DOI":"10.14814\/phy2.70558","type":"journal-article","created":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T08:55:57Z","timestamp":1758272157000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>MK2<\/scp> deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction"],"prefix":"10.14814","volume":"13","author":[{"given":"Jo\u00eblle","family":"Tr\u00e9panier","sequence":"first","affiliation":[{"name":"Montreal Heart Institute  Montr\u00e9al Qu\u00e9bec Canada"},{"name":"Department of Biochemistry and Molecular Medicine Universit\u00e9 de Montr\u00e9al  Montr\u00e9al Qu\u00e9bec Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sherin 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