Key result
Mathematical modeling suggests limited cytokinesis in S-phase adult cardiomyocytes drives low intrinsic myocardial regeneration.
Why the study?
Although adult mammalian myocardial renewal is low, recent studies identified genetic variants impacting cardiomyocyte cell cycle reentry, prompting modeling of regenerative growth.
Computational modeling suggests that the inability of adult cardiomyocytes to complete cytokinesis, rather than failure to reenter the cell cycle, limits myocardial regeneration.
Cautions against assuming cell-cycle reentry alone drives regeneration; leaves open whether cytokinesis enhancement improves adult myocardial repair.
Although the myocardial renewal rate in the adult mammalian heart is quite low, recent studies have identified genetic variants which can impact the degree of cardiomyocyte cell cycle reentry. Here we use the compound interest law to model the level of regenerative growth over time in mice exhibiting different rates of cardiomyocyte cell cycle reentry following myocardial injury. The modeling suggests that the limited ability of S-phase adult cardiomyocytes to progress through cytokinesis, rather than the ability to reenter the cell cycle per se, is a major contributor to the low levels of intrinsic regenerative growth in the adult myocardium.
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Soonpaa et al. (2023) studied Myocardial injury. Compound interest law modeling was evaluated on Level of regenerative growth over time. Mathematical modeling suggests the limited ability of S-phase adult cardiomyocytes to progress through cytokinesis is a major contributor to low intrinsic regenerative growth in the adult myocardium.
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