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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2018,5,15]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Pressure overload triggers responses in cardiomyocytes and noncardiomyocytes, leading to pressure overload hypertrophy (POH). Here, we show that cardiac resident macrophages regulate compensatory myocardial adaptation to POH, while nonresident infiltrating macrophages are detrimental. At early-phase POH, pressure overload induces cardiac resident macrophage proliferation, which is regulated by Kruppel-like factor 4. At late-phase POH, pressure overload also induces Ly6C\n                    <jats:sup>hi<\/jats:sup>\n                    monocyte infiltration, and its blockade improves myocardial angiogenesis and preserves cardiac function. Mechanistically, the differential impact of these two macrophage subsets on myocardial angiogenesis may underlie the cardiac phenotype. These findings provide insights regarding the role of cardiac resident and nonresident macrophages, conceptually update the view of myocardial angiogenesis, and identify monocyte infiltration as a therapeutic target for nonischemic cardiomyopathy.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1720065115","type":"journal-article","created":{"date-parts":[[2018,4,30]],"date-time":"2018-04-30T15:17:04Z","timestamp":1525101424000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":183,"title":["Distinct roles of resident and nonresident macrophages in nonischemic cardiomyopathy"],"prefix":"10.1073","volume":"115","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8864-0755","authenticated-orcid":false,"given":"Xudong","family":"Liao","sequence":"first","affiliation":[{"name":"Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH 44106;"},{"name":"Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2496-3077","authenticated-orcid":false,"given":"Yuyan","family":"Shen","sequence":"additional","affiliation":[{"name":"Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH 44106;"},{"name":"Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rongli","family":"Zhang","sequence":"additional","affiliation":[{"name":"Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH 44106;"},{"name":"Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Keiki","family":"Sugi","sequence":"additional","affiliation":[{"name":"Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH 44106;"},{"name":"Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neelakantan T.","family":"Vasudevan","sequence":"additional","affiliation":[{"name":"Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, OH 44106;"},{"name":"Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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