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-β1after 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-β1 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-β1. TUG1 knockdown suppressed the biological process of cardiac fibroblasts treated with TGF-β1 by sponging miR-590.

心脏纤维化与急性心肌梗死 (AMI) 后的心肌重塑有关，可导致心力衰竭、心律失常甚至心源性猝死。研究急性心肌梗死 (AMI) 中心脏纤维化的分子机制对于更好地了解这种病理学至关重要。本研究旨在探讨 TUG1 对 AMI 后心脏纤维化的影响，并阐明 AMI 的潜在分子机制。将大鼠随机分为4组（假手术组、心肌梗死组（AMI组）、si-NC治疗组和si-TUG1治疗组）。使用细胞计数试剂盒 8 (CCK8) 和 Transwell 测定法评估 TGF-β1 处理的心脏成纤维细胞在转染 si-TUG1 或 miR-590 模拟物或 miR-590 抑制剂或 FGF1 模拟物或组合后的生物学行为。SatarBase v2.0 用于预测目标 microRNA 与 TUG1 和 FGF1 的结合位点候选者。使用蛋白质印迹和恢复实验来探索潜在的机制。TUG1 表达上调，并且 TUG1 的敲低改善了 AMI 大鼠的心脏功能。TUG1 的敲低抑制了细胞活力和迁移，并改善了 TGF-β1 处理的心脏成纤维细胞的胶原蛋白生成。SatarBase v2.0 显示 TUG1 充当 miR-590 的海绵，而 FGF1 是 miR-590 的直接靶标。TUG1 表达在 AMI 组织和用 TGF-β1 处理的心脏成纤维细胞中增加。