Myocardial infarction (MI) is a common cardiovascular disease characterized by an interruption of blood and oxygen supply to the heart, which results in gradual damage to the myocardial tissue and ultimately heart failure. The role of long non‐coding RNAs in the pathology of MI remains in its infancy, but has been implicated in MI and other heart conditions. For example, the expression of a non‐coding RNA hypoxia‐inducible factor 1α (HIF1A)‐antisense RNA 2 (HIF1A‐AS2) has previously been linked to coronary heart disease, however, whether HIF1A‐AS2 expression is also high in MI has not been addressed. Here, we report that HIF1A‐AS2 is upregulated in hypoxia‐treated human cardiomyocytes (HMCs) compared with normal cardiomyocytes, and that silenced HIF1A‐AS2 inhibited apoptosis and facilitated viability, migration, and invasion of HMCs. Our data suggested that in MI, HIF1A‐AS2 upregulation was associated with miR‐623, which promoted expression of tripartite motif containing 44 (TRIM44). Moreover, by upregulating TRIM44 we were able to remedy the HIF1A‐AS2 repression of apoptosis in HMCs. Thus, we conclude that cardiomyocytes can be protected against hypoxic‐treated injury by knockdown of HIF1A‐AS2, which suppresses TRIM44, and that HIF1A‐AS2 overexpression is a prognostic indicator of MI.

中文翻译：

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击倒HIF1A-AS2可抑制TRIM44，以保护心肌细胞免受缺氧引起的损伤。

心肌梗塞（MI）是一种常见的心血管疾病，其特征是心脏血液和氧气供应中断，从而导致心肌组织逐渐受损，最终导致心力衰竭。长期的非编码RNA在MI病理中的作用仍处于婴儿期，但与MI和其他心脏病有关。例如，以前非编码RNA缺氧诱导因子1α（HIF1A）-反义RNA 2（HIF1A-AS2）的表达与冠心病有关，但是，MI中HIF1A-AS2的表达是否也很高没有解决。在这里，我们报告说，与正常心肌细胞相比，低氧处理的人心肌细胞（HMC）中的HIF1A-AS2被上调，而沉默的HIF1A-AS2则抑制了细胞凋亡并促进了HMC的活力，迁移和侵袭。我们的数据表明，在MI中，HIF1A-AS2的上调与miR-623相关，miR-623促进了包含44（TRIM44）的三方基序的表达。此外，通过上调TRIM44，我们能够纠正HIF1A-AS2对HMC细胞凋亡的抑制作用。因此，我们得出的结论是，可以通过敲低HIF1A-AS2抑制TRIM44来保护心肌细胞免受低氧治疗损伤，并且HIF1A-AS2的过表达是MI的预后指标。