Physiological and pathological cardiac hypertrophy
- •Pathological and physiological hypertrophy differs in the signaling pathways that drive these processes.
- •Pathological hypertrophy develops myocytes death and fibrotic remodeling, and this promotes systolic and diastolic dysfunction.
- •Besides cell autonomous mechanisms, interaction between cardiomyocytes and non-cardiomyocytes modulates cardiomyocyte hypertrophy.
The heart must continuously pump blood to supply the body with oxygen and nutrients. To maintain the high energy consumption required by this role, the heart is equipped with multiple complex biological systems that allow adaptation to changes of systemic demand. The processes of growth (hypertrophy), angiogenesis, and metabolic plasticity are critically involved in maintenance of cardiac homeostasis. Cardiac hypertrophy is classified as physiological when it is associated with normal cardiac function or as pathological when associated with cardiac dysfunction. Physiological hypertrophy of the heart occurs in response to normal growth of children or during pregnancy, as well as in athletes. In contrast, pathological hypertrophy is induced by factors such as prolonged and abnormal hemodynamic stress, due to hypertension, myocardial infarction etc. Pathological hypertrophy is associated with fibrosis, capillary rarefaction, increased production of pro-inflammatory cytokines, and cellular dysfunction (impairment of signaling, suppression of autophagy, and abnormal cardiomyocyte/non-cardiomyocyte interactions), as well as undesirable epigenetic changes, with these complex responses leading to maladaptive cardiac remodeling and heart failure. This review describes the key molecules and cellular responses involved in physiological/pathological cardiac hypertrophy.
Keywords:Cardiac hypertrophy, Heart failure, Angiogenesis, Akt, Autophagy, Inflammation, Epigenetic modification,MicroRNA, Metabolism
Autor / Fonte:Ippei Shimizu, Tohru Minamino Journal of Molecular and Cellular Cardiology 2016 June 1