Heart failure is the end-stage of many heart diseases with poor prognosis, and its risk increases significantly with age and myocardial cell aging. The mammalian target of rapamycin (mTOR) pathway plays a key role in the pathophysiology of cardiomyocyte aging. This article reviews the latest research progress of the mTOR pathway in heart failure caused by myocardial cell aging, and explores potential intervention strategies to delay cardiomyocyte aging. This article shows that the continued activation of mTORC1 during aging drives pathological cardiac changes and accelerates the progression of heart failure by regulating protein synthesis, lipid metabolism, and inhibiting autophagy. Conversely, inhibiting the overactivation of mTORC1 can slow cardiac aging and extend lifespan in elderly animals. This article provides new insights into alleviating heart failure caused by aging and could help reduce the societal burden of this disease.

心力衰竭是多种心脏疾病的终末期阶段，预后较差，其发病风险随年龄增长和心肌细胞衰老而显著增加。哺乳动物雷帕霉素靶蛋白（mTOR）通路在心肌细胞衰老的病理生理学中发挥关键作用。本文综述了mTOR通路在心肌细胞衰老引起心力衰竭中的最新研究进展，并探讨了延缓心肌细胞衰老的干预策略。心肌细胞衰老过程中mTOR复合物1（mTORC1）的持续激活通过调节蛋白质合成、脂质代谢和抑制自噬等机制，驱动心脏病理性改变并加速心力衰竭的发生、发展；而抑制mTORC1的过度激活能够延缓老年动物的心脏衰老进程并延长寿命。本文为缓解衰老引起的心力衰竭提供了新的见解，有助于减轻社会的疾病负担。