Cardiac hypertrophy commonly occurs in response to pathological conditions such as hypertension and myocardial infarction from coronary artery disease, which eventually give rise to ventricular remodelling and dilatation, fibrosis, and diminished cardiac output 2, 3. As a consequence, although cardiac mass can be increased by fibroblast proliferation, and possibly also by progenitor cell activity and some cardiomyocyte renewal, mass increase primarily occurs through the hypertrophy of individual cardiomyocytes ( BOX 1). Unlike other cell types that comprise the heart (that is, endothelial cells, fibroblasts, immune cells and progenitor cells), mammalian cardiomyocytes become terminally differentiated shortly after birth and mostly lose their ability to proliferate, although a low level of cardiomyocyte turnover occurs throughout life 1, 4, 5. Cardiomyocytes, which represent 85% of the heart mass, are the contracting cells of the heart, and they contain an arrayed series of basic contractile units called sarcomeres 1– 3 ( BOX 1). However, hypertrophy, from the Greek for ‘increased growth’, is a more complex phenomenon than this simple definition might suggest. In response to an increased workload, typically caused by pathological or physiological stimulation, the heart undergoes a growth process named hypertrophy, which decreases ventricular wall stress and maintains or even augments pump function ( BOX 1). The mammalian heart is a muscle, the fundamental function of which is to pump blood throughout the circulatory system to deliver oxygen and nutrients to organs and to transport carbon dioxide back to the lungs.
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