We know quite a lot about how cardiomyocytes develop and mature and now recognise that they  continue to divide throughout life. Less is known about what happens to individual myocytes as they age, but we recognise global ventricular fibrosis and diminishing function. Whilst attempts to enhance regeneration or reverse senescence have been disappointing, a simple increase in daily activity seems to have a beneficial effect on the ageing heart.

Over the last decade the Chaudhry/Henderson research group have been using zebrafish to study how the heart ages, why fibrosis occurs and if long term increased activity in adulthood prevents the changes of ageing. We found that, as in people, cardiomyocyte proliferation in the zebrafish continues throughout life, but discovered programmed cell death suddenly accelerates in middle age and is then followed by fibrosis. This is “good fibrosis” as it fills in the holes made by lost cardiomyocytes. We found that whilst long term exercise gave the fish stronger hearts, it also led to increased levels of myocardial fibrosis, which might lead to other problems such as atrial fibrillation. In addition, we also found that the ability of cardiomyocytes to proliferate in response to stressful situations diminishes with age and exercise has no effect on this. Exercise gives us healthier hearts, but cannot turn back the clock on cardiomyocyte ageing. Read the full study in the journal Disease Models and Mechanisms.

For more information contact Bill Chaudhry or Deborah Henderson

Lindsay B. Murphy, Adrian Santos-Ledo, Tamilvendhan Dhanaseelan, Lorraine Eley, David Burns, Deborah J. Henderson, Bill Chaudhry. Exercise, programmed cell death and exhaustion of cardiomyocyte proliferation in aging zebrafish. Dis Model Mech (2021) 14 (7): dmm049013

 This work was funded by the British Heart Foundation

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