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].