{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T23:09:33Z","timestamp":1790896173341,"version":"4.1.0"},"reference-count":44,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:p> We investigated sex differences and the role of estrogen receptor-\u03b2 (ER\u03b2) on myocardial hypertrophy in a mouse model of pressure overload. We performed transverse aortic constriction (TAC) or sham surgery in male and female wild-type (WT) and ER\u03b2 knockout (ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup>) mice. All mice were characterized by echocardiography and hemodynamic measurements and were killed 9 wk after surgery. Left ventricular (LV) samples were analyzed by microarray profiling, real-time RT-PCR, and histology. After 9 wk, WT males showed more hypertrophy and heart failure signs than WT females. Notably, WT females developed a concentric form of hypertrophy, while males developed eccentric hypertrophy. ER\u03b2 deletion augmented the TAC-induced increase in cardiomyocyte diameter in both sexes. Gene expression profiling revealed that WT male hearts had a stronger induction of matrix-related genes and a stronger repression of mitochondrial genes than WT female hearts. ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup> mice exhibited a different transcriptional response. ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup>\/TAC mice of both sexes exhibited induction of proapoptotic genes with a stronger expression in ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup> males. Cardiac fibrosis was more pronounced in male WT\/TAC than in female mice. This difference was abolished in ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup> mice. The number of apoptotic nuclei was increased in both sexes of ER\u03b2<jats:sup>\u2212\/\u2212<\/jats:sup>\/TAC mice, most prominent in males. Female sex offers protection against ventricular chamber dilation in the TAC model. Both female sex and ER\u03b2 attenuate the development of fibrosis and apoptosis, thus slowing the progression to heart failure. <\/jats:p>","DOI":"10.1152\/ajpregu.00825.2009","type":"journal-article","created":{"date-parts":[[2010,4,8]],"date-time":"2010-04-08T01:48:28Z","timestamp":1270691308000},"page":"R1597-R1606","source":"Crossref","is-referenced-by-count":230,"title":["Female sex and estrogen receptor-\u03b2 attenuate cardiac remodeling and apoptosis in pressure overload"],"prefix":"10.1152","volume":"298","author":[{"given":"Daniela","family":"Fliegner","sequence":"first","affiliation":[{"name":"Institute of Gender in Medicine and"},{"name":"Center for Cardiovascular Research, Charit\u00e9-Medical University Berlin;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carola","family":"Schubert","sequence":"additional","affiliation":[{"name":"Institute of Gender in Medicine and"},{"name":"Center for Cardiovascular Research, Charit\u00e9-Medical University 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