{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T20:51:03Z","timestamp":1777927863156,"version":"3.51.4"},"reference-count":0,"publisher":"SAGE Publications","issue":"6","license":[{"start":{"date-parts":[[2009,12,1]],"date-time":"2009-12-01T00:00:00Z","timestamp":1259625600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["OMICS: A Journal of Integrative Biology"],"published-print":{"date-parts":[[2009,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>We have previously found that CHF1\/Hey2 prevents the development of phenylephrine-induced cardiac hypertrophy. To determine the role of CHF1\/Hey2 in pressure overload hypertrophy, we performed ascending aortic banding on wild-type and transgenic mice overexpressing CHF1\/Hey2 in the myocardium. We found that both wild-type and transgenic mice developed increased ventricular weight to body weight ratios 1 week after aortic banding. Wild-type mice also developed decreased fractional shortening after 1 week when compared to preoperative echocardiograms and sham-operated controls. Transgenic mice, in comparison, demonstrated preserved fractional shortening. Histological examination of explanted heart tissue demonstrated extensive fibrosis in wild-type hearts, but minimal fibrosis in transgenic hearts. TUNEL staining demonstrated increased apoptosis in the wild-type hearts but not in the transgenic hearts. Exposure of cultured neonatal myocytes from wild-type and transgenic animals to hydrogen peroxide, a potent inducer of apoptosis, demonstrated increased apoptosis in the wild-type cells. Gene Set Analysis of microarray data from wild-type and transgenic hearts 1 week after banding revealed suppression and activation of multiple pathways involving apoptosis, cell signaling, and biosynthesis. These findings demonstrate that CHF1\/Hey2 promotes physiological over pathological hypertrophy through suppression of apoptosis and regulation of multiple transcriptional pathways. These findings also suggest that CHF1\/Hey2 and its downstream pathways provide a variety of targets for novel heart failure drug discovery, and that genetic polymorphisms in CHF1\/Hey2 may affect susceptibility to hypertrophy and heart failure.<\/jats:p>","DOI":"10.1089\/omi.2009.0086","type":"journal-article","created":{"date-parts":[[2009,12,15]],"date-time":"2009-12-15T17:36:16Z","timestamp":1260898576000},"page":"501-511","source":"Crossref","is-referenced-by-count":10,"title":["CHF1\/Hey2 Promotes Physiological Hypertrophy in Response to Pressure Overload through Selective Repression and Activation of Specific Transcriptional Pathways"],"prefix":"10.1177","volume":"13","author":[{"given":"Man","family":"Yu","sequence":"first","affiliation":[{"name":"University of Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yonggang","family":"Liu","sequence":"additional","affiliation":[{"name":"University of Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fan","family":"Xiang","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yuxin","family":"Li","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Darragh","family":"Cullen","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ronglih","family":"Liao","sequence":"additional","affiliation":[{"name":"Brigham and Women's Hospital"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Richard P.","family":"Beyer","sequence":"additional","affiliation":[{"name":"University of Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Theodor K.","family":"Bammler","sequence":"additional","affiliation":[{"name":"University of Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael T.","family":"Chin","sequence":"additional","affiliation":[{"name":"University of Washington"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"179","published-online":{"date-parts":[[2009,12]]},"container-title":["OMICS: A Journal of Integrative Biology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1089\/omi.2009.0086","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1089\/omi.2009.0086","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T22:55:09Z","timestamp":1777676109000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/full\/10.1089\/omi.2009.0086"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2009,12]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[2009,12]]}},"alternative-id":["10.1089\/omi.2009.0086"],"URL":"https:\/\/doi.org\/10.1089\/omi.2009.0086","relation":{},"ISSN":["1536-2310","1557-8100"],"issn-type":[{"value":"1536-2310","type":"print"},{"value":"1557-8100","type":"electronic"}],"subject":[],"published":{"date-parts":[[2009,12]]}}}