心脏再生 z-bo 2020-09-22 665

　　Search studies have shown that the chromosomal ends of cardiomyocytes are quickly eroded after birth, which limits the cell's ability to proliferate and replace damaged heart tissue. The research and paper also propose new interventions that can improve the heart's ability to repair the heart after a heart attack. Newborns can repair injured heart muscles, but in adults, heart disease can cause permanent damage, often leading to heart failure and death. Newborn mice can also regenerate damaged heart tissue.

　　Their cardiomyocytes can proliferate and repair the heart in the first week after birth, but as mice age, they lose the ability to regenerate, and most of the cardiomyocytes end their cell cycle. Researchers want to know whether the cause of cell cycle arrest is related to telomeres, which are repetitive DNA sequences that protect the ends of chromosomes. If telomeres become too short (for example, loss of telomere elongation, telomerase), the cell will mistake the end of the chromosome for damaged DNA fragments, leading to checkpoints that inhibit cell cycle activation. Therefore, Flores et al. checked the chromosomal telomere length of the cardiomyocytes of newborn mice and found that the telomeres were rapidly eroded in the first week after birth. This erosion is consistent with decreased telomerase expression, DNA damage response, and activation of a cell cycle inhibitor called p21. Compared with wild-type mice, telomerase-deficient mice have shorter telomeres, and the researchers found that their cardiomyocytes stopped growing during the first day of life.

　　When Flores and his colleagues injured the heart of a 1-day-old mouse, telomerase-deficient cardiomyocytes were unable to proliferate or regenerate the damaged heart muscle. In contrast, wild-type cardiomyocytes can proliferate and replace damaged tissue. They also found that knocking out the cell cycle inhibitor p21 can prolong the regeneration of cardiomyocytes. Compared with 1-week-old wild-type mice, 1-week-old p21-deficient mice can repair damaged hearts more effectively. Organization. Therefore, maintaining the telomere length of cardiomyocytes can increase the regeneration capacity of adult cells, which can improve the recovery of heart tissue during a heart attack. Flores said: "We are preparing a mouse model of telomerase overexpression to study whether this regeneration range can be expanded."