TUG1 knockdown suppresses cardiac fibrosis after myocardial infarction

Cardiac fibrosis is involved in myocardial remodeling following acute myocardial infarction (AMI), which can result in heart failure, arrhythmias and even sudden cardiac death. Investigating the molecular mechanisms of cardiac fibrosis in acute myocardial infarction (AMI) is essential for better understanding this pathology. The current study aims to investigate the effect of TUG1 on cardiac fibrosis after AMI and elucidated the underlying molecular mechanism of AMI. Rats were randomly divided into four groups (sham-operation group, myocardial infarction group (AMI group), si-NC treated group and si-TUG1 treated group). The biological behavior of cardiac fibroblasts treated with TGF-beta 1after being transfected by si-TUG1 or miR-590 mimic or miR-590 inhibitor or FGF1 mimic or a combination was evaluated using the cell counting kit-8 (CCK8) and Transwell assays. SatarBase v2.0 was used to predict the target microRNAs binding site candidates with TUG1 and FGF1. Western blot and recovery experiments were used to explore the potential mechanism. TUG1 expression was up-regulated and knockdown of TUG1 improved cardiac function in AMI rats. Knockdown of TUG1 suppressed cell viability and migration and improved collagen production of TGF-beta 1 treated cardiac fibroblasts. SatarBase v2.0 showed TUG1 served as a sponge for miR-590 and FGF1 is a direct target of miR-590. TUG1 expression was increased in AMI tissue and cardiac fibroblasts treated with TGF-beta 1. TUG1 knockdown suppressed the biological process of cardiac fibroblasts treated with TGF-beta 1 by sponging miR-590.

Automated summary

This study aims to investigate the impact of TUG1 on cardiac fibrosis following acute myocardial infarction (AMI) and elucidate the underlying molecular mechanism. The results demonstrate that knockdown of TUG1 improves cardiac function in AMI rats and suppresses the biological behavior of cardiac fibroblasts. Furthermore, TUG1 acts as a sponge for miR-590 and is involved in regulating the process of cardiac fibrosis.