{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T07:43:55Z","timestamp":1791272635941,"version":"4.1.0"},"reference-count":28,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2003,7,8]]},"abstract":"<jats:p>\n            <jats:bold>\n              <jats:italic>Background\u2014<\/jats:italic>\n            <\/jats:bold>\n            Preconditioning phenomena provide evidence for adaptive responses to ischemia that have important implications for treatment\/prevention of myocardial infarction. Hypoxia-inducible factor 1 (HIF-1) mediates adaptive transcriptional responses to hypoxia\/ischemia.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Methods and Results\u2014<\/jats:italic>\n            <\/jats:bold>\n            Exposure of wild-type mice to intermittent hypoxia resulted in protection of isolated hearts against ischemia-reperfusion injury 24 hours later. Cardiac protection induced by intermittent hypoxia was lost in\n            <jats:italic>Hif1a<\/jats:italic>\n            <jats:sup>\n              <jats:italic>+\/<\/jats:italic>\n              \u2212\n            <\/jats:sup>\n            mice heterozygous for a knockout allele at the locus encoding HIF-1\u03b1. Erythropoietin (EPO) mRNA expression was induced in kidneys of wild-type mice subjected to intermittent hypoxia, resulting in increased plasma EPO levels. EPO mRNA expression was not induced in\n            <jats:italic>Hif1a<\/jats:italic>\n            <jats:sup>\n              <jats:italic>+\/<\/jats:italic>\n              \u2212\n            <\/jats:sup>\n            mice. EPO administration to rats increased functional recovery and decreased apoptosis in isolated hearts subjected to ischemia-reperfusion 24 hours later.\n          <\/jats:p>\n          <jats:p>\n            <jats:bold>\n              <jats:italic>Conclusions\u2014<\/jats:italic>\n            <\/jats:bold>\n            Hearts isolated from rodents subjected to intermittent hypoxia or EPO administration are protected against postischemic injury. Cardiac protection induced by intermittent hypoxia is critically dependent on\n            <jats:italic>Hif1a<\/jats:italic>\n            gene dosage. Our data suggest that additional studies to evaluate therapeutic applications of EPO administration are warranted.\n          <\/jats:p>","DOI":"10.1161\/01.cir.0000078635.89229.8a","type":"journal-article","created":{"date-parts":[[2003,6,10]],"date-time":"2003-06-10T07:32:59Z","timestamp":1055230379000},"page":"79-85","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":441,"title":["Hearts From Rodents Exposed to Intermittent Hypoxia or Erythropoietin Are Protected Against Ischemia-Reperfusion Injury"],"prefix":"10.1161","volume":"108","author":[{"given":"Zheqing","family":"Cai","sequence":"first","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dominador J.","family":"Manalo","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guo","family":"Wei","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E. Rene","family":"Rodriguez","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karen","family":"Fox-Talbot","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huasheng","family":"Lu","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay L.","family":"Zweier","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregg L.","family":"Semenza","sequence":"additional","affiliation":[{"name":"From the McKusick-Nathans Institute of Genetic Medicine (Z.C., D.J.M., G.L.S.), Division of Cardiology, Department of Medicine (G.W., J.L.Z.), and Department of Pathology (E.R.R., K.F.-T.), Johns Hopkins University School of Medicine, Baltimore, 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