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Conversely, myostatin overexpression induced an approximately 20% decrease in cardiomyocyte size and blocked the hypertrophic response to PE.
These alterations in cardiac mass were accompanied by a corresponding increase or decrease in cardiomyocyte size and Akt and NFAT3 activity in the myostatin inhibition and overexpression groups, respectively.
This has been associated with a decrease in cardiomyocyte size.
Both RNAi therapies induced a decrease in cardiomyocyte size.
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Importantly, limited hypertrophy in TGJ1ICD hearts after TAC was associated with a significant reduction in cardiomyocyte size.
Cardiomyocytes also undergo hypertrophic growth, defined as an increase in cardiomyocyte size above that which occurs at any given stage of post-natal mammalian growth [1], [2].
TG-9 hearts displayed a marked increase in cardiomyocyte size indicating cellular hypertrophy (Fig. 2G and 2H).
Differences in cardiomyocyte size between control rats and HFD rats, however, were not observed.
Since the increase in cardiomyocyte size and heart weight was about 20 30% (Bry et al, 2010), this indicated an increased arteriole/cardiomyocyte-ratio.
Furthermore, dislocation of HKII from the mitochondria results in an increase in cardiomyocyte size due to elevated ROS production.
Interestingly, this aging-induced increase in cardiomyocyte size was not seen in the cathepsin K knockout mice (Fig. 3A, B).
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