期刊
CELL CYCLE
卷 2, 期 3, 页码 220-223出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.2.3.381
关键词
Cardiac; Signal transduction; Kinase; Apoptosis; Growth; Hypertrophy
类别
资金
- NIH [HL-59521, HL-61557, HL-04250]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL061557, R01HL059521] Funding Source: NIH RePORTER
In many systems, activation of the protein and lipid kinase phosphoinositide 3-kinase (PI 3-kinase) and its downstream serine-threonine kinase effector, Akt (or Protein Kinase B), provide a potent stimulus for cell proliferation, growth, and survival. In the heart, constrained by the limited proliferative capacity of cardiomyocytes, this pathway plays a key role in regulating cardiomyocyte growth and survival, with little effect on proliferation. Simultaneously, PI 3-kinase and Akt are important modulators of metabolic substrate utilization and cardiomyocyte function. Thus, the convergent signaling pathways controlling so many clinically important phenotypes of the cardiomyocyte suggest it holds promise as a therapeutic target in a variety of cardiac diseases. However, the similar role of PI 3-kinase/Akt signaling in neoplasia suggests the difficulty of activating this pathway in the heart without invoking adverse consequences elsewhere. Here we review evidence regarding the role of PI 3-kinase/Akt in controlling cardiomyocyte growth and survival, and discuss the implications for therapeutic strategies.
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