2.1.2 Chemical stimuli
A recent study by Ceylan-Isik et al. showed that
autophagy-related protein levels of beclin 1, Atg5, Atg7, and LC3-II
were observably decreased and hypertrophic markers such as
aminopeptidase N (ANP), transcription factor GATA4 and phosphorylated
nuclear factor of activated T cells 3 (NFATc3), was activated in H9c2
myoblasts induced by endothelin-1 (ET-1), which is a polypeptide of 21
amino acids [34]. Chen et al. revealed that decreasing of
connexin 43, a key protein involved in information transmission among
organizations, can attenuate the expression of LC3-II and increase cell
death and apoptosis in Ang II-treated H9c2 cells [35]. Another
report showed that High-fat diet (HFD) decreased autophagy activity and
increased cardiac hypertrophy, fibrosis, and apoptosis [36]. Similar
to HFD, Guo et al. found that ethanol can induce the accumulation
of acetaldehyde and autophagosomes, then promote cardiac hypertrophy.
However, ethanol can also reduce compensatory wall thickening in the
hearts of pressure-overloaded (PO) mice [37-39]. These chemical
stimuli share a common feature that deteriorates cardiac hypertrophy by
altering autophagic levels. Therefore, myocardial hypertrophy can be
prevented by targeting these chemical stimuli.