Cell polyploidy. Cardiac muscle. Liver. Ontogenesis and regeneration

Cell (somatic) polyploidy is a general biological phenomenon characteristic of unicellular and multicellular animals and plants. In mammals, polyploid cells occur in all tissues; in some cases they are few in number, while in other cases they may be the most numerous cells in an organ. The mechanism of polyploidization is a usual, but incomplete, mitosis. The cause of incompletion of the mitosis is competition between proliferation and differentiation. At the genome level, the cause is associated with metabolic disorders of cyclin-dependent kinases, some other mitotic kinases (AURORA), transcription factors Ect2, E2F, some regulatory proteins (p53, laminin, septin), and components of the Hippo signalling pathway. The timing of polyploidization is restricted to early postnatal ontogenesis and, as experiments with heart transplants have shown, is part of the developmental programme. A typical way of genome multiplication is the change from binucleate to polyploid mononucleate cells from cycle to cycle. Polyploidization of cells is irreversible. It is a normal mechanism of organ growth and, for some cells, a way of differentiation. Using cardiac muscle and liver as examples, it has been shown that the composition and number of polyploid cells depend on the life conditions in the early postnatal period. After leaving the mitotic cycle, the cells continue to grow; postmitotic hypertrophy is one of the main ways of the growth of the cardiac muscle in ontogenesis and the only way of its regeneration. A certain growth reserve of the cardiac muscle in case of damage (heart attack, etc.) has been revealed, which is associated with its ploidy formed in childhood. In case of damage to mammalian liver, all hepatocytes enter the cycle and both cell division and polyploidization occur. Polyploidy in the course of ontogenesis up to the stage of aging fully complements the restoration of tissue and organ activity.