The molecular mechanisms involved in the transition of cardiac hypertrophy to heart failure (HF) are not fully characterized. Autophagy is a catabolic, self-renewal intracellular mechanism, which protects the heart during HF. In the heart of a mouse model of angiotensin-II-induced hypertrophy, Sun and colleagues demonstrated that reduced levels of miR-93 lead to synaptotagmin-7 (Syt-7) upregulation and consequent inhibition of autophagy. miR-93 overexpression or syt-7 inhibition rescues autophagy and maladaptive hypertrophy. This research identifies new players in the pathophysiology of cardiac hypertrophy, opening innovative therapeutic perspectives. miR-93 may also be considered in the future as a novel circulating biomarker for patients at high risk to develop HF.

中文翻译：

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miR-93 和 synaptotagmin-7：心脏肥大期间调节自噬的两个新参与者

心脏肥大转变为心力衰竭（HF）的分子机制尚未完全表征。自噬是一种分解代谢、自我更新的细胞内机制，可在心力衰竭期间保护心脏。Sun 及其同事在血管紧张素 II 诱导的肥大小鼠模型的心脏中证明，miR-93 水平降低会导致突触结合蛋白 7 (Syt-7) 上调，从而抑制自噬。miR-93 过表达或 syt-7 抑制可挽救自噬和适应不良肥大。这项研究确定了心脏肥大病理生理学的新参与者，开辟了创新的治疗视角。未来，miR-93 也可能被视为心力衰竭高风险患者的新型循环生物标志物。