Abstract
Cardiac hypertrophy is a result of cardiac response to excessive heart burden. The sustention of hypertrophic stress indicates a higher risk of cardiac failure or even sudden death. Despite the increasing research works on cardiac hypertrophy, there remains a considerable space left for further mechanism exploration. Long noncoding RNAs (lncRNAs) are a cluster of transcripts lacking in protein coding potential. Past decades have witnessed the increasing identification of their significant roles in cardiac hypertrophy. Small nucleolar RNA host gene 7 (SNHG7) has been identified as an oncogene in human cancers, but its function in cardiac hypertrophy remains unknown. SDA1 domain containing 1 (SDAD1) is newly discovered to exert procancer function in several cancers, whose role in cardiac hypertrophy remains elusive. Present study sought to investigate the biological function of SNHG7 in cardiac hypertrophy. First, the expressions of SNHG7 and SDAD1 were found to be upregulated in Ang II-induced cardiac hypertrophy model in the neonatal rat cardiomyocytes (NRCMs). Functionally, loss-of-function assays verified that silencing SNHG7 and SDAD1 attenuated the inductive effect of Ang II on cardiac hypertrophy. Mechanistically, we proved that SNHG7 interacted with Hu Antigen R so as to stabilize SDAD1 messenger RNA (mRNA). In conclusion, this study proved that SNHG7 facilitates cardiac hypertrophy via the stabilization of SDAD1 mRNA, indicating SNHG7 as a novel regulator for cardiac hypertrophy.