BACKGROUND: The @entity9829 family of @entity9829 ( @entity9829 ) transcription factors ( @entity9829 , @entity27619 , and @entity42598 ) is involved in fundamental biological processes such as proliferation, apoptosis, @entity5 angiogenesis, and @entity1184 . The role of individual @entity9829 transcription factors in the stressed heart is not clear. In the present study we analyzed the role of @entity42598 in survival, @entity1184 , and angiogenesis in the pressure-overloaded @entity19 heart after thoracic aortic constriction. METHODS AND RESULTS: @entity19 lacking @entity42598 (knockout [KO]) showed increased mortality and enhanced @entity66 and @entity82 associated with increased levels of @entity519 -induced factor-1alpha, @entity1611 ( @entity1611 ), @entity899 , and @entity1380 protein and reduced levels of @entity1379 protein after 7 days of severe pressure overload compared with @entity164 ( @entity164 ) siblings. Cardiomyocyte @entity1184 in surviving KO @entity19 was enhanced compared with that in @entity164 @entity19 . Chronic moderate pressure overload for 12 weeks caused enhanced @entity4346 in KO @entity19 , and survival and interstitial @entity82 were comparable with @entity164 @entity19 . Cardiac function, 12 weeks after operation, was comparable among shams and pressure-overloaded @entity19 of both genotypes. In addition, KO @entity19 exposed to chronic pressure overload showed higher cardiac capillary density associated with increased protein levels of @entity1611 . CONCLUSIONS: Thus, @entity42598 limits cardiomyocyte @entity1184 and protects the pressure-overloaded heart from cardiac apoptosis. These beneficial effects of @entity42598 , however, are associated with antiangiogenic properties.

Lack of @entity42598 promotes pressure overload-induced apoptosis, XXXX growth, and angiogenesis in the heart.

@entity27619 :: ('16477(Tax:10090)', 'Gene') :: ['JunB'] @entity1380 :: ('12028(Tax:10090)', 'Gene') :: ['Bax'] @entity82 :: ('MESH:D005355', 'Disease') :: ['fibrosis'] @entity66 :: ('MESH:D004194', 'Disease') :: ['cardiomyocyte apoptosis'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophy'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity19 :: ('10090', 'Species') :: ['mice', 'Mice', 'mouse'] @entity899 :: ('22060(Tax:10090)', 'Gene') :: ['p53'] @entity42598 :: ('16478(Tax:10090)', 'Gene') :: ['JunD'] @entity519 :: ('MESH:D000860', 'Disease') :: ['hypoxia'] @entity4346 :: ('MESH:D017379', 'Disease') :: ['left ventricular hypertrophy'] @entity164 :: ('MESH:D017827', 'Disease') :: ['wild-type', 'WT'] @entity1379 :: ('12043(Tax:10090)', 'Gene') :: ['Bcl-2'] @entity1611 :: ('22339(Tax:10090)', 'Gene') :: ['VEGF', 'vascular endothelial growth factor'] @entity9829 :: ('16476(Tax:10090)', 'Gene') :: ['activator protein 1', 'Jun', 'AP-1', 'c-Jun']
@entity1184 :: (MESH:D006984,Disease) :: ['hypertrophic']
