Heart failure (HF) is associated with a considerable number of symptoms and significantly impaired health for humans, including reduced quality of life and physical functioning. Previous studies have indicated that miRNAs have important roles in regulating the development of HF. MiR-1180 is involved in the proliferation, migration, invasiveness, and chemoresistance of cancer cells; however, the underlying mechanisms and role of miR-1180 in the functioning of cardiomyocytes remains unclear. In this study, we found that miR-1180 promotes cell activity and cell cycle processes by driving energy generation through NKIRAS2, which declines over time during development. The expression of miR-1180 is down-regulated in cells subjected to hypoxia-reoxygenation, and use of an miR-1180 mimic significantly reduced myocardial injury and cell apoptosis. In addition, miR-1180 regulates the NFκB pathway through NKIRAS2 in cardiomyocytes. These findings suggest that miR-1180 maybe a novel therapeutic target for use in getting cardiomyocytes to re-enter the cell cycle as well as for cardiac repair following myocardial injury.

中文翻译：

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MiR-1180通过NKIRAS2-NFκB途径促进损伤后的心肌细胞周期再进入。

心力衰竭（HF）与大量症状相关，并严重损害人类健康，包括生活质量和身体机能下降。先前的研究表明，miRNA在调节HF的发展中具有重要作用。MiR-1180与癌细胞的增殖，迁移，侵袭性和化学抗性有关。然而，miR-1180在心肌细胞功能中的潜在机制和作用仍不清楚。在这项研究中，我们发现miR-1180通过驱动NKIRAS2产生能量来促进细胞活性和细胞周期过程，而NKIRAS2在发育过程中会随着时间而下降。miR-1180的表达在进行缺氧-复氧的细胞中被下调，miR-1180模拟物的使用显着降低了心肌损伤和细胞凋亡。另外，miR-1180通过心肌细胞中的NKIRAS2调节NFκB途径。这些发现表明，miR-1180可能是一种新颖的治疗靶标，可用于使心肌细胞重新进入细胞周期以及心肌损伤后进行心脏修复。