2.2.2 Inhibition or activation of specific proteins
As the complicated mechanism of cardiac hypertrophy, the changes of many
enzymes, proteins, and proteasomes may inhibit the pathogenesis of
cardiac hypertrophy. Ba et al . reported that nucleotide-binding
oligomerization domain (NOD)-like receptor family CARD domain containing
5 (NLRC5), as a nuclear receptor, ameliorated cardiac hypertrophy
through enhancing autophagy via inactivation of Akt/mTOR pathway
[65]. Cao et al. found that the inhibition of histone
deacetylases (HDACs) by trichostatin A (TSA), a broad-spectrum HDAC
deacetylase family inhibitor, repressed cardiac autophagy and decreased
cardiomyocyte hypertrophy in C57BL/6 mice subjected by TAC [33]. Qiet al. showed that in response to pathological stimuli, the
anti-hypertrophic and anti-autophagic effects of myostatin (MSTN), a
protein for inhibiting the growth of skeletal muscle, were associated
with the direct inhibition of AMPK/mTOR and activation of the peroxisome
proliferator-activated receptor-gamma (PPARγ)/nuclear factor-κB (NF-κB)
signaling pathway [66]. Another report showed that immunoproteasome
catalytic subunit b5i interacted with Atg5 and promoted its degradation,
then inhibited autophagy and cardiac hypertrophy [67].