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].