{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T04:00:31Z","timestamp":1772164831276,"version":"3.50.1"},"reference-count":95,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"4","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2021,2,16]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Mitogen\u2010activated protein kinase\u2013activated protein kinase\u20102 (MK2) is a protein serine\/threonine kinase activated by p38\u03b1\/\u03b2. Herein, we examine the cardiac phenotype of pan MK2\u2010null (MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) mice.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Survival curves for male MK2\n                      <jats:sup>+\/+<\/jats:sup>\n                      and MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice did not differ (Mantel\u2010Cox test,\n                      <jats:italic>P<\/jats:italic>\n                      =0.580). At 12 weeks of age, MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice exhibited normal systolic function along with signs of possible early diastolic dysfunction; however, aging was not associated with an abnormal reduction in diastolic function. Both R\u2010R interval and P\u2010R segment durations were prolonged in MK2\u2010deficient mice. However, heart rates normalized when isolated hearts were perfused ex vivo in working mode. Ca\n                      <jats:sup>2+<\/jats:sup>\n                      transients evoked by field stimulation or caffeine were similar in ventricular myocytes from MK2\n                      <jats:sup>+\/+<\/jats:sup>\n                      and MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice had lower body temperature and an age\u2010dependent reduction in body weight. mRNA levels of key metabolic genes, including\n                      <jats:italic>Ppargc1a<\/jats:italic>\n                      ,\n                      <jats:italic>Acadm<\/jats:italic>\n                      ,\n                      <jats:italic>Lipe<\/jats:italic>\n                      , and\n                      <jats:italic>Ucp3,<\/jats:italic>\n                      were increased in hearts from MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. For equivalent respiration rates, mitochondria from MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      hearts showed a significant decrease in Ca\n                      <jats:sup>2+<\/jats:sup>\n                      sensitivity to mitochondrial permeability transition pore opening. Eight weeks of pressure overload increased left ventricular mass in MK2\n                      <jats:sup>+\/+<\/jats:sup>\n                      and MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice; however, after 2\u00a0weeks the increase was significant in MK2\n                      <jats:sup>+\/+<\/jats:sup>\n                      but not MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice. Finally, the pressure overload\u2013induced decrease in systolic function was attenuated in MK2\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice 2\u00a0weeks, but not 8\u00a0weeks, after constriction of the transverse aorta.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Collectively, these results implicate MK2 in (1) autonomic regulation of heart rate, (2) cardiac mitochondrial function, and (3) the early stages of myocardial remodeling in response to chronic pressure overload.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.120.017791","type":"journal-article","created":{"date-parts":[[2021,2,3]],"date-time":"2021-02-03T06:56:22Z","timestamp":1612335382000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":8,"title":["MK2\u2010Deficient Mice Are Bradycardic and Display Delayed Hypertrophic Remodeling in Response to a Chronic Increase in Afterload"],"prefix":"10.1161","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4583-9718","authenticated-orcid":false,"given":"Matthieu","family":"Ruiz","sequence":"first","affiliation":[{"name":"Department of Medicine Universit\u00e9 de Montr\u00e9al Qu\u00e9bec Canada"},{"name":"Montreal Heart Institute Montr\u00e9al Qu\u00e9bec Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maya","family":"Khairallah","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Medicine Universit\u00e9 de Montr\u00e9al 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