心力衰竭是多种心脏疾病进展至终末期的表现，代谢重构是引起心力衰竭的重要机制，探寻新型代谢重构调控因子对心力衰竭的治疗具有重要意义。T-UCR（超保守区转录本）是一类由基因组中超高保守区域转录产生的长链非编码RNA，其高度保守性提示其可能具有重要生物学功能。我们前期研究发现：沉默T-UCR uc.323可显著促进苯肾上腺素诱导的心肌肥厚；uc.323基因敲除小鼠在12周龄时即出现自发性心肌肥厚，伴随心功能明显下降；并且，uc.323表达下调导致多个脂肪酸和糖代谢的关键调控因子显著下调，提示uc.323可能通过影响代谢重构调控心力衰竭。由于目前尚无uc.323与心力衰竭的研究，因此，本研究拟通过基因敲除小鼠、小干扰RNA及腺病毒转染等技术，深入探讨uc.323对心力衰竭的调控作用及其分子机制，旨在阐明改善代谢重构是否为uc.323抑制心力衰竭的核心机制，以为心力衰竭的治疗提供新的理论依据。

Heart failure is a common end-stage manifestation of various cardiovascular diseases. Metabolic remodeling plays a crucial role in the pathogenesis of heart failure, therefore it’s of great clinical significance to explore novel metabolic remodeling regulators. T-UCR (Transcribed Ultraconserved Region) transcripts are highly conserved long non-coding RNA (lnRNA). Our preliminary data showed that silencing T-UCR uc.323 can significantly promote phenylephrine-induced cardiac hypertrophy. Spontaneous cardiac hypertrophy occurs in uc.323 knockout mice at 12 weeks of age, accompanied with a significant decline in cardiac function. Furthermore, the down-regulation and deletion of uc.323 results in significant down-regulation of multiple fatty acid and carbohydrate metabolism regulatory genes, suggesting that uc.323 may improve heart failure through regulating metabolic remodeling. However, the role of uc.323 in heart failure remains unknown. Therefore, in this study, with uc.323 knockout mice, small interfering RNA and adenovirus transfection technology, we aim to explore the regulatory effects of uc.323 on heart failure, in order to clarify whether metabolic remodeling improvement is the core mechanism and target of uc.323 in the regulation of heart failure. Our study may provide theoretical basis for the treatment of heart failure.