LncRNA-MHRT介导声动力疗法对心肌梗死后心脏功能的保护作用及机制研究

Heart failure is a common complication after myocardial infarction. The prevention of heart failure has important significance to reduce cardiac disease mortality rates. At present, LncRNA and autophagy are important targets in the research of cardiovascular diseases. Sonodynamic therapy (SDT) is a hotspot in the treatment field of cardiovascular disease. It has been reported that SDT can activate autophagy and inhibit atherosclerosis, nevertheless, the exact role of SDT involved in myocardial infarction-induced heart failure is unknown. Our previous studies showed that SDT could inhibit the differentiation and proliferation of myocardial fibroblasts and reduce collagen synthesis in myocardial tissue. SDT could inhibit cardiac fibrosis and improve cardiac function after myocardial infarction. Moreover, SDT has protective effect on cardiac myocytes. Therefore, we propose that SDT may regulate LncRNA-MHRT expression and promote autophagy of cardiomyocytes, which inhibit cardiomyocyte apoptosis and treat heart failure after myocardial infarction. To confirm the above hypothesis, we will elucidate the effect and mechanism of SDT in the treatment of heart failure after myocardial infarction in vitro and in vivo, which are evaluated using the technology of molecular biology, cytology and pathology. In conclusion, the study will have new insight into development of treatment methods with independent intellectual property rights to prevent and treat heart failure after myocardial infarction.

心力衰竭是心肌梗死后常见的并发症，研究其防治对降低心血管病致死率具有重要意义。目前，LncRNA及自噬是心血管疾病研究领域的重要靶点；声动力疗法（SDT）是心血管疾病治疗领域的热点，已报道SDT能够激活自噬抑制动脉粥样硬化，但其对心肌梗死后心力衰竭的作用尚不清楚。我们在前期工作中发现：SDT可以抑制心肌成纤维细胞分化及增殖、减少心肌组织内胶原合成，抑制心脏纤维化，进而改善心肌梗死后的心脏功能；同时发现SDT干预心肌细胞后，具有保护细胞的作用。因此，我们提出假设：SDT通过调控LncRNA-MHRT表达促进心肌细胞自噬，抑制心肌细胞凋亡，治疗心肌梗死后心力衰竭。为了证实这一假设，我们将通过细胞和大鼠模型，利用分子生物学、细胞学及病理学等技术方法，从分子、细胞及动物水平探讨SDT治疗心肌梗死后心力衰竭的作用及机制。通过本课题将为研发具有自主知识产权的治疗方法防治心肌梗死后心力衰竭奠定理论基础。

心力衰竭是心肌梗死后常见的并发症，研究其防治对降低心血管病致死率具有重要意义。目前，LncRNA及自噬是心血管疾病研究领域的重要靶点；声动力疗法（SDT）是心血管疾病治疗领域的热点，已报道SDT能够激活自噬抑制动脉粥样硬化，但其对心肌梗死后心力衰竭的作用尚不清楚。我们在前期工作中发现：SDT可以抑制心肌成纤维细胞分化及增殖、减少心肌组织内胶原合成，抑制心脏纤维化，进而改善心肌梗死后的心脏功能；同时发现SDT干预心肌细胞后，具有保护细胞的作用。因此，我们提出假设：SDT通过调控LncRNA-MHRT表达促进心肌细胞自噬，抑制心肌细胞凋亡，治疗心肌梗死后心力衰竭。为了证实这一假设，我们将通过细胞和大鼠模型，利用分子生物学、细胞学及病理学等技术方法，从分子、细胞及动物水平探讨SDT治疗心肌梗死后心力衰竭的作用及机制。通过本课题将为研发具有自主知识产权的治疗方法防治心肌梗死后心力衰竭奠定理论基础。