Role of the insulin-like growth factor 1 (IGF1)/phosphoinositide-3-kinase (PI3K) pathway mediating physiological cardiac hypertrophy.
Growth of the heart can be induced by physiological stimuli (e.g. postnatal development or chronic exercise training: 'the athlete's heart') or pathological stimuli (e.g. pressure or volume overload). Physiological hypertrophy is characterized by the normal organization of sarcomeres and fibres, normal or enhanced cardiac function and a relatively normal pattern of cardiac gene expression; whereas pathological hypertrophy is associated with an altered pattern of cardiac gene expression, fibrosis, cardiac dysfunction and increased mortality. Previously, an unresolved question in cardiac biology was whether distinct signalling pathways are responsible for the development of pathological and physiological cardiac hypertrophy. Recent studies have identified several signalling pathways that play unique roles in the regulation of pathological and physiological cardiac hypertrophy. This review focuses largely on the role of the insulin-like growth factor 1 (IGF1)/phosphoinositide-3-kinase (PI3K) pathway in mediating physiological cardiac growth.
McMullen
Julie R
JR
Baker Heart Research Institute, Melbourne, Victoria, Australia.
Izumo
Seigo
S
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology*; D005786:Gene Expression Regulation; D006801:Humans; D007334:Insulin-Like Growth Factor I / Q000378:metabolism / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D008954:Models, Biological; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000378:metabolism; D015398:Signal Transduction
D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D038744:Ribosomal Protein S6 Kinases, 90-kDa