Molecular and cellular mechanisms of mechanical stress-induced cardiac hypertrophy.
Congestive heart failure is one of the major issues for cardiologists. Since cardiac hypertrophy deteriorates into heart failure, it is important to elucidate the mechanisms of cardiac hypertrophy. Hemodynamic overload, namely mechanical stress, is a major cause for cardiac hypertrophy. Mechanical stress induces various hypertrophic responses such as activation of phosphorylation cascades of many protein kinases, expression of specific genes and an increase in protein synthesis. During this process, secretion and production of vasoactive peptides such as angiotensin II and endothelin-1, are increased and play critical roles in the induction of these hypertrophic responses. Recently, a Ca2+ dependent protein kinase, CaMK, and a Ca2+ dependent protein phosphatase, calcineurin, have attracted great attention as critical molecules that induce cardiac hypertrophy. In this review, we described the mechanisms by which mechanical stress induces cardiac hypertrophy, especially focusing on the role of calcineurin in the development of cardiac hypertrophy.
Zou
Yunzeng
Y
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Inohana, Japan.
Takano
Hiroyuki
H
Akazawa
Hiroshi
H
Nagai
Toshio
T
Mizukami
Miho
M
Komuro
Issei
I
D000804:Angiotensin II / Q000502:physiology; D019703:Calcineurin / Q000502:physiology; D002118:Calcium / Q000502:physiology; D006332:Cardiomegaly / Q000209:etiology* / Q000503:physiopathology; D019332:Endothelin-1 / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D011494:Protein Kinases / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013314:Stress, Mechanical; D017871:Calcium-Calmodulin-Dependent Protein Kinases
D000804:Angiotensin II; D019703:Calcineurin; D002118:Calcium; D019332:Endothelin-1; D011494:Protein Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases