We examined the role of @entity19729 in the development of @entity65 using @entity19729 knockout (KO) @entity19 . 1. Pressure overload and mechanical stretch induced @entity1184 responses in KO and wild type (WT) cardiomyocytes (CM). Stretch activated MAPK through PKC in @entity164 and through @entity669 kinase in KO CM. 2. The number of @entity1540 and @entity591 was larger in WT @entity19 than KO @entity19 . 3. Left ventricular remodeling after @entity583 was more remarkable in WT @entity19 than KO @entity19 . 4. @entity1317 induced neointimal formation in KO @entity19 as well as in WT @entity19 .

[The role of angiotensin II in the development of XXXX ].

@entity583 :: ('MESH:D009203', 'Disease') :: ['myocardial infarction'] @entity19 :: ('10090', 'Species') :: ['mice'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophic'] @entity591 :: ('MESH:D013610', 'Disease') :: ['tachycardia'] @entity164 :: ('MESH:D017827', 'Disease') :: ['WT CM'] @entity1540 :: ('MESH:D018879', 'Disease') :: ['ventricular premature beats'] @entity1317 :: ('MESH:D057772', 'Disease') :: ['Vascular injury'] @entity19729 :: ('11607(Tax:10090)', 'Gene') :: ['AT1', 'AT1a'] @entity669 :: ('CHEBI:18186', 'Chemical') :: ['tyrosine'] @entity65 :: ('MESH:D002318', 'Disease') :: ['cardiovascular remodeling']
@entity65 :: (MESH:D002318,Disease) :: ['cardiovascular remodeling']
