Insulin signaling: a possible pathogenesis of cardiac hypertrophy.
Cardiac hypertrophy is one of the most commonly cardiovascular diseases in clinical practice. Despite the extensive studies, the pathophysiology of cardiac hypertrophy, however, remains incompletely understood. Studies have demonstrated that insulin signaling may be involved in cardiac growth and protein synthesis. More recently, a growing body of evidence suggests that insulin signaling is associated with the development of cardiac hypertrophy. The evidence for the hypotheses included that (1) several studies have demonstrated insulin is an important regulator of physiological cardiac growth; (2) PI3K-Akt pathway has been investigated as a participant in the cardiac hypertrophic program; (3) negative regulators of insulin signaling show beneficial effects on cardiac hypertrophy development; and (4) insulin signaling interaction with angiotensin II in cardiac hypertrophy. Although the studies suggest that the association between insulin signaling and cardiac hypertrophy, the exact pathogenesis of insulin signaling in cardiac hypertrophy development remains elusive and requires further investigation. Insulin signaling may provide a scientific basis for further research on the underlying mechanisms of cardiac hypertrophy and may target for pharmacological interruption of cardiac hypertrophy.
Yu
Wei
W
Department of Cardiology, The First Affiliated Hospital of Shantou University Medical College, Shantou, PR China.
Chen
Chunjuan
C
Fu
Yucai
Y
Wang
Xin
X
Wang
Wei
W
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D015398:Signal Transduction
D007328:Insulin; D000804:Angiotensin II; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt