Experimental studies suggest that the @entity262 ( @entity262 ) and its primary effector peptide, @entity15395 ( @entity15395 ), are involved in the pathophysiology of @entity1283 and failure. All the components required for @entity15395 production are present in the heart, and cardiac @entity15395 formation appears to be regulated independent from the circulating @entity262 . In animal models and in @entity1 with @entity712 , the cardiac @entity262 is activated and, presumably, local @entity15395 formation is enhanced. Several cardiac cell types express @entity15395 type 1 ( @entity19729 ) and/or type 2 ( @entity19730 )-receptors and represent potential targets for @entity15395 -mediated effects. In neonatal cardiac myocytes, @entity15395 induces a @entity1184 response via the @entity14207 . Likewise, activation of the @entity14207 triggers @entity1184 in terminally differentiated cardiac myocytes and in perfused heart preparations. In the neonatal system, @entity15395 appears to be a major autocrine/paracrine mediator of cardiac myocyte @entity1184 in response to passive mechanical stretch. By contrast, @entity14207 activation apparently is not required to trigger load-induced @entity1184 in the adult cardiomyocyte. Recent studies suggest that the @entity19728 opposes @entity14207 -mediated growth signals in neonatal and in adult cardiac myocytes. Pharmacological studies have established that a blockade of the @entity262 at the level of the @entity14206 ( @entity14206 ) or the @entity14207 ameliorates the remodeling process of the heart and prolongs long-term survival in animal models of @entity1283 and failure. The therapeutic effects of @entity14206 inhibitors and @entity14207 antagonists clearly suggest an important role for the @entity14206 - @entity15395 - @entity14207 axis in the development of @entity1283 and failure. It must be kept in mind, however, that these drugs enhance @entity19728 and B2-kinin receptor-dependent signaling pathways which may contribute significantly to the beneficial effects observed in vivo. Molecular and physiological analyses of @entity19 with a cardiac-specific overexpression of the @entity19729 or @entity19728 confirm that @entity19729 and @entity19728 -dependent signaling cascades potently modulate cardiac myocyte function and growth. However, studies in @entity14207 knockout @entity19 demonstrate that @entity1283 in response to hemodynamic overload can occur independent from the @entity14207 . In this paper, we review recent experimental evidence suggesting a critical role for the @entity262 in @entity1283 and failure with special emphasis on the putative role of @entity15395 signaling in cardiac myocytes.

The @entity262 and experimental XXXX .

@entity1 :: ('9606', 'Species') :: ['patients'] @entity712 :: ('MESH:D006333', 'Disease') :: ['heart failure'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophic', 'hypertrophy'] @entity15395 :: ('11606(Tax:10090)', 'Gene') :: ['Ang II and Ang II-receptor', 'angiotensin II', 'Ang II'] @entity1283 :: ('MESH:D006332', 'Disease') :: ['cardiac hypertrophy'] @entity19 :: ('10090', 'Species') :: ['mice', 'transgenic mice'] @entity262 :: ('MESH:D034721', 'Disease') :: ['RAS', 'renin-angiotensin system'] @entity19728 :: ('11609(Tax:10090)', 'Gene') :: ['AT2-receptor'] @entity14206 :: ('11421(Tax:10090)', 'Gene') :: ['ACE', 'angiotensin-converting enzyme'] @entity19730 :: ('20726(Tax:10090)', 'Gene') :: ['AT2'] @entity19729 :: ('11607(Tax:10090)', 'Gene') :: ['AT1'] @entity14207 :: ('11610(Tax:10090)', 'Gene') :: ['AT1-receptor']
@entity712 :: (MESH:D006333,Disease) :: ['heart failure']
