Physiological and pathological cardiac 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.
Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan; Division of Molecular Aging and Cell Biology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan. Electronic address: ippeishimizu@yahoo.co.jp.
Ippei
I
Shimizu
Department of Cardiovascular Biology and Medicine, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan. Electronic address: t_minamino@yahoo.co.jp.
Tohru
T
Minamino
D000818:Animals; D001343:Autophagy; D006332:Cardiomegaly / Q000175:diagnosis / Q000209:etiology* / Q000378:metabolism*; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000175:diagnosis / Q000209:etiology / Q000378:metabolism; D006801:Humans; D009389:Neovascularization, Pathologic; D018919:Neovascularization, Physiologic; D012307:Risk Factors; D015398:Signal Transduction
Akt; Angiogenesis; Autophagy; Cardiac hypertrophy; Epigenetic modification; Heart failure; Inflammation; Metabolism; MicroRNA