Differential activation of stress-response signaling in load-induced cardiac hypertrophy and failure.

ABSTRACT: Hypertrophic growth of the myocardium occurs in most forms of heart failure and may contribute to the pathogenesis of the failure state. Little is known about the regulatory mechanisms governing the often-coexisting phenotypes of hypertrophy, systolic failure, and diastolic stiffness that characterize clinical disease. We hypothesized that intracellular signaling pathways are differentially activated by graded degrees of hemodynamic stress. To test this, we developed models of graded pressure stress in mice and used them to directly compare compensated hypertrophy and pressure-overload heart failure. Surgical interventions were designed to be similar, on either side of a threshold separating compensated from decompensated responses. Our findings revealed two dramatically different hypertro

SUBMITTER: Rothermel BA 

PROVIDER: S-EPMC4118287 | biostudies-literature | 2005 Sep

REPOSITORIES: biostudies-literature