Molecular determinants of the physiological adaptation to stress in the cardiomyocyte: a focus on AKT.
Cardiomyocytes (CMCs) adapt to physiological or pathological stimuli by undergoing molecular changes which differentiate according to the specificity of the stimulus and eventually generate a phenotype with peculiar molecular characteristics. Here, we review the literature on the molecular mechanisms activated in the CMC during physiologic adaptation to stress, as opposed to maladaptation. The critical role of the IGF-1 receptor/PI3K/Akt signaling pathway during this process is described, including effector targets regulating inotropism and cell size.
Ceci
Marcello
M
San Raffaele Biomedical Science Park, Rome 00128, Italy.
Ross
John
J
Condorelli
Gianluigi
G
D000222:Adaptation, Physiological; D000818:Animals; D007334:Insulin-Like Growth Factor I / Q000502:physiology*; D051379:Mice; D032383:Myocytes, Cardiac / Q000201:enzymology* / Q000378:metabolism / Q000502:physiology; D017346:Protein Serine-Threonine Kinases / Q000502:physiology*; D011518:Proto-Oncogene Proteins / Q000502:physiology*; D051057:Proto-Oncogene Proteins c-akt; D015398:Signal Transduction; D013312:Stress, Physiological / Q000201:enzymology*
D011518:Proto-Oncogene Proteins; D007334:Insulin-Like Growth Factor I; D017346:Protein Serine-Threonine Kinases; D051057:Proto-Oncogene Proteins c-akt