Abstract:
:Biomechanical stress is a major stimulus for cardiac hypertrophy and the transition to heart failure. By generating mice that harbor a ventricular restricted knockout of the gp130 cytokine receptor via Cre-IoxP-mediated recombination, we demonstrate a critical role for a gp130-dependent myocyte survival pathway in the transition to heart failure. Such conditional mutant mice have normal cardiac structure and function, but during aortic pressure overload, these mice display rapid onset of dilated cardiomyopathy and massive induction of myocyte apoptosis versus the control mice that exhibit compensatory hypertrophy. Thus, cardiac myocyte apoptosis is a critical point in the transition between compensatory cardiac hypertrophy and heart failure. gp130-dependent cytokines may represent a novel therapeutic strategy for preventing in vivo heart failure.
journal_name
Celljournal_title
Cellauthors
Hirota H,Chen J,Betz UA,Rajewsky K,Gu Y,Ross J Jr,Müller W,Chien KRdoi
10.1016/s0092-8674(00)80729-1subject
Has Abstractpub_date
1999-04-16 00:00:00pages
189-98issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80729-1journal_volume
97pub_type
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