Paternal sleep deprivation and cardiac dysfunction in offspring: A perspective of myocardial hypertrophy

The objective of this work is to assess the effects and potential process of paternal acute sleep deprivation on cardiac function in their offspring. Male and female C57BL/6N mice aged 8–9 weeks ( n = 4–5 mice/group) were used. Male mice were selected to construct an acute sleep deprivation model using the modified multiple platform method (MMPM) and mated with normal female mice. After gestation, the weight change of offspring mice was observed and recorded. At the time of 10 weeks, the changes of cardiac function were evaluated by blood pressure, heart rate and echocardiography; cardiac histology and cytopathological changes were observed by haematoxylin–eosin staining; and the molecular mechanism induced by acute paternal sleep deprivation were further elucidated by molecular biological techniques. In the acute sleep deprivation group, male offspring showed significant cardiac hypertrophy, whereas female offspring did not. mRNA levels of GATA binding protein 4 (GATA4) ( P < 0.01) and mRNA levels of classic hypertrophic genes, such as atrial natriuretic peptide (ANP) ( P < 0.05) and brain natriuretic peptide (BNP) ( P < 0.05), increased significantly in the hearts of the acute sleep deprivation group. Paternal acute sleep deprivation may lead to cardiac dysfunction in offspring through cardiac hypertrophy.