2.2.1 microRNAs
miRNAs can not only promote cardiac hypertrophy but also inhibit
physiological and pathological cardiac hypertrophy through inhibiting
autophagy. The reason is probably that different lengths of miRNAs have
a different effect on cardiomyocytes, resulting in seemingly
contradictory situations that miRNAs can both promote or inhibit
myocardial hypertrophy. A recent study by Huang et al. showed
that in an Ang II-induced rat model of cardiomyocytes, miR-34a
attenuates cardiomyocytes hypertrophy through inhibiting the expression
of Atg9A, which is the only transmembrane Atg proteins involved in
forming autophagosomes [60, 61]. Accordingly, the above inhibitory
effect of miR-34a on cardiac hypertrophy through inhibiting Atg9A
expression suggested that miR-34a-targeted Atg9A may be a new target for
treating cardiac hypertrophy [62]. Qi et al. found that in
pressure-overloaded induced rat hearts, miR-103, which is often regarded
as a negative regulator for HF specifically through inhibiting target
transient receptor potential vanilloid 3 (TRPV3) to decrease cardiac
autophagic flux and the protein levels of hypertrophic markers (BNP and
β-MHC), could partially alleviate cardiac hypertrophy [63, 64].
Similar result has been reported by Qi et al. used in vivo and in
vitro models of cardiac hypertrophy induced by swimming and IGF-1,
respectively [31]. The research showed that overexpressed
miR-26b-5p, miR-204-5p and miR-497-3p attenuated the expression of
hypertrophic mRNA levels (ANP and BNP), and significantly reduced the
autophagy related protein levels of Atgs (ULK1, LC3B and beclin 1)
[31].