Heart failure preceded by pathological cardiac hypertrophy is a leading cause of death. Long noncoding RNA small nucleolar RNA host gene 1 (SNHG1) was reported to inhibit cardiomyocytes apoptosis, but the role and underlying mechanism of SNHG1 in pathological cardiac hypertrophy have not yet been understood. This study was designed to investigate the role and molecular mechanism of SNHG1 in regulating cardiac hypertrophy. We found that SNHG1 was upregulated during cardiac hypertrophy both in vivo (transverse aortic constriction treatment) and in vitro (phenylephrine [PE] treatment). SNHG1 overexpression attenuated the cardiomyocytes hypertrophy induced by PE, while SNHG1 inhibition promoted hypertrophic response of cardiomyocytes. Furthermore, SNHG1 and high‐mobility group AT‐hook 1 (HMGA1) were confirmed to be targets of miR‐15a‐5p. SNHG1 promoted HMGA1 expression by sponging miR‐15a‐5p, eventually attenuating cardiomyocytes hypertrophy. There data revealed a novel protective mechanism of SNHG1 in cardiomyocytes hypertrophy. Thus, targeting of SNHG1‐related pathway may be therapeutically harnessed to treat cardiac hypertrophy.

中文翻译：

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LncRNA SNHG1通过靶向miR-15a-5p / HMGA1轴在心肌肥大中发挥保护作用

继发于病理性心脏肥大的心力衰竭是死亡的主要原因。据报道，长非编码RNA小核仁RNA宿主基因1（SNHG1）抑制心肌细胞凋亡，但尚不清楚SNHG1在病理性心肌肥大中的作用和潜在机制。本研究旨在研究SNHG1在调节心脏肥大中的作用和分子机制。我们发现SNHG1在心肌肥大过程中在体内（横向主动脉收缩治疗）和体外（去氧肾上腺素[PE]治疗）均被上调。SNHG1的过表达减轻了PE诱导的心肌肥大，而SNHG1的抑制则促进了心肌的肥大反应。此外，SNHG1和高机动性AT-hook 1组（HMGA1）被证实是miR-15a-5p的靶标。SNHG1通过使miR-15a-5p海绵化而促进HMGA1表达，最终减轻心肌肥大。那里的数据揭示了SNHG1在心肌肥大中的新型保护机制。因此，可以在治疗上利用SNHG1相关途径的靶向来治疗心脏肥大。