Telomerase reverse transcriptase (TERT) promotes the expression of the enzyme telomerase, which is responsible for copying the ends of chromosomes known as telomeres. Maintaining telomere length is necessary for the growth, survival, and injury prevention of cells. But, after birth, TERT production normally stops in most cell types. Consequently, telomeres are incapable of unlimited proliferation as they shorten during the aging process. Researchers at the Baylor College of Medicine, Waco, Texas, have engineered mice to produce TERT at levels found only in embryonic cells (O. Hidemasa et al., "Telomerase reverse transcriptase promotes cardiac muscle cell proliferation, hypertrophy, and survival," Proceedings of the National Academy of Sciences, 98, 10308-13, Aug. 28, 2001.) Forcing TERT expression in the mice showed a reduced loss of telomerase activity in postmitotic myocardium, maintenance of telomere length, and delay in cardiac cell exit. After proliferation ceased, hypertrophy (cell enlargement) took place. But, hypertrophy's normal adverse...
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