LC3B is a marker of autophagic activity, and growing evidence supports its importance in myocardial hypertrophy. Thus, regulating LC3B expression may provide an important avenue to inhibit autophagy and protect against or inhibit pathological myocardial hypertrophy. To address this question, we investigated the effects of altering LC3B mRNA expression and autophagic activity in the setting of cardiomyocyte hypertrophy. In an in vitro angiotensin II (Ang II)-induced cardiomyocyte hypertrophy model, LC3B mRNA and protein expression was increased and there was activation of cardiomyocyte autophagy, which was assessed by transmission electron microscopy and flow cytometry. LC3B cDNA transfection also resulted in an upregulation of autophagic activity, whereas downregulation of autophagic activity was observed with knockdown of LC3B expression. Induction of LC3B expression was shown to further exacerbate Ang II-stimulated cardiomyocyte hypertrophy, whereas inhibition of LC3B expression inhibited the Ang II-stimulated cardiomyocyte hypertrophy (as assessed through cardiomyocyte morphology and expression of ANP and β-MHC). This study demonstrated that LC3B modulates the Ang II-induced cardiomyocyte hypertrophy in cultured neonatal rat ventricular cardiomyocytes.

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It has been suggested that renal denervation (RD) may attenuate left ventricular (LV) hypertrophy. However, the role that autophagy serves in this process is currently unclear. In the present study, utilizing a model of hypertension-induced cardiac hypertrophy in spontaneous hypertensive rats, it was demonstrated that RD was significantly associated with a reduction in LV hypertrophy. Furthermore, a decrease in the myocardial mRNA of hypertrophy-associated genes was demonstrated in RD rats compared with sham controls. In addition, RD in hypertension-induced LV hypertrophy rats was associated with the attenuation of cellular autophagic response over activation at a physiological level. This was indicated by a reduction in the expression of Beclin-1, autophagy related 9A and microtubule-associated protein 1A/1B-light chain 3 II/I in RD rats to physiological levels that are observed in control rats. Furthermore, the number of autophagosomes was restored to physiological levels in the cardiomyocytes of RD rats. The results of the current study suggest that RD may attenuate LV hypertrophy via the regulation of autophagic responses.