心脏衰老（cardiac aging, CA）是诱发心力衰竭和心脏骤亡的重要原因，高盐摄入（high-salt intake, HSI）能加速CA及相关疾病的发生，而运动训练（exercise training, ET）能延缓CA并抵抗相关疾病，其分子通路均可能与Insulin信号通路、氧化应激、TOR通路等有关。果蝇Salt（人类SLC5A12）基因决定细胞的盐敏感性，对细胞衰老有重要调控作用，但心脏salt基因是否介导HSI、ET对CA的调控，仍然未知。该项目首先构建果蝇ET模型、HSI模型、心肌salt基因特异性RNAi和过表达，通过分析心脏结构、功能、及CA相关的分子通路的增龄变化情况，证实心肌salt基因在CA中的作用，阐明ET与HSI调控CA的机制，并筛选ET对抗HSI诱发、salt基因表达缺陷诱发CA的关键分子通路，为ET联合心肌salt基因对抗CA及其相关疾病提供理论依据。

Cardiac aging (CA) is an important cause of heart failure and cardiac death. High salt intake (HSI) can accelerate the occurrence of CA and related diseases, while exercise training (ET) can delay CA and resist related diseases. The molecular pathways may be related to the Insulin signaling pathway, oxidative stress, and TOR pathway.The Salt (human SLC5A12) gene is closely related to the Salt sensitivity of cells and is also involved in the regulation of cell aging. However, it is still unknown whether the heart Salt gene mediates the regulation of HSI and ET on CA.This project firstly builds flies ET model, HSI model, myocardial salt gene specificity RNAi and express. And then, to confirm the role of myocardial salt genes in CA, and to clarify the mechanism of ET and HSI regulation of CA, the cardiac structure and function, the CA, and the age change related molecular pathways are measured. Finally, screening the key molecular pathways of ET against HIS and CA induced salt gene defects. Providing the theoretical basis for ET combined with myocardial salt gene to fight CA and related diseases.