《生命科学》 2025, 37(9): 1160-1172

Apelin/APJ系统在肌少症中的主要作用机制及研究进展

王　浩^1,2 , 王浩哲^1,2 , 王　欢^1,2 , 方文君^1,2 , 李梦欠^1,2 , 王惠国^1,2,* , 朱　琳^1,3,* , 刘晓光^1,2,*

¹广州体育学院运动与健康学院，广州 515000 ²广州体育学院体卫融合创新发展研究中心， 广州 510500 ³粤港澳大湾区体育科学创新研究中心，广州体育学院，广州 510500

摘　要：

肌少症是骨骼肌质量和功能进行性下降的退行性疾病，严重影响生活质量。爱帕琳肽(Apelin) 是G 蛋白偶联受体APJ 的内源性配体，在组织中广泛表达。在骨骼肌中，Apelin/APJ 系统通过磷脂酰肌醇3-激酶/ 蛋白激酶B  (phosphatidylinositol 3-kinase-protein kinase B, PI3K/Akt) 促进蛋白质合成、抑制肌萎缩基因并增强修复能力；通过AMP 激活的蛋白激酶(AMP-activated protein kinase, AMPK) 调节线粒体生物合成与脂肪酸氧化以改善能量代谢；通过抑制核因子κB (nuclear factor kappa B, NF-κB) 缓解慢性炎症；还能通过血管内皮细胞生长因子(vascular  endothelial growth factor, VEGF) 刺激内皮型一氧化氮合酶(endothelial nitric oxide synthase, eNOS) 生成改善血管功能，间接修复骨骼肌。衰老、骨骼肌低活动状态、营养摄入不足、激素水平减退等因素会降低Apelin 的表达量，进而加剧肌少症的发展。Apelin 在废用性骨骼肌萎缩、代谢性骨骼肌萎缩以及肌营养不良症等骨骼肌疾病中也通过 PI3K/Akt、AMPK 和NF-κB 等通路改善肌萎缩。本文旨在阐述Apelin 的结构、分布及在肌少症中的表达调节机制，明确Apelin 改善骨骼肌功能与质量的作用途径，为靶向治疗提供理论支持。

通讯作者：王惠国 , Email:wanghuiguo163@163.com 朱　琳 , Email:11251@gzsport.edu.cn 刘晓光 , Email:liuxg@gzsport.edu.cn

The main mechanisms of action and research progress of the Apelin/APJ system in sarcopenia

WANG Hao^1,2 , WANG Hao-Zhe^1,2 , WANG Huan^1,2 , FANG Wen-Jun^1,2 , LI Meng-Qian^1,2 , WANG Hui-Guo^1,2,* , ZHU Lin^1,3,* , LIU Xiao-Guang^1,2,*

¹School of Sport and Health, Guangzhou Sport University, Guangzhou 510500, China ²Research Center for Innovative Development of Sports and Healthcare Integration, Guangzhou Sport University, Guangzhou 510500, China ³Innovative Research Center for Sports Science in the Guangdong-Hong Kong-Macao Greater Bay Area, Guangzhou Sport University, Guangzhou 510500, China

Abstract:

Sarcopenia is a degenerative disease characterized by progressive decline in skeletal muscle mass and function, severely affecting quality of life. Apelin, an endogenous ligand for the G protein-coupled receptor APJ, is widely expressed in tissues. In skeletal muscle, the Apelin/APJ system promotes protein synthesis, inhibits muscle atrophy genes, and enhances repair capacity via the phosphatidylinositol 3-kinase-protein kinase B (PI3K/Akt) pathway; regulates mitochondrial biogenesis and fatty acid oxidation to improve energy metabolism through AMPactivated protein kinase (AMPK); reduces chronic inflammation by inhibiting nuclear factor kappa B (NF-κB); and improves vascular function by stimulating endothelial nitric oxide synthase (eNOS) via vascular endothelial growth factor (VEGF), thereby indirectly repairing skeletal muscle. Factors such as aging, reduced skeletal muscle activity, insufficient nutritional intake, and  decreased hormone levels decrease Apelin expression, exacerbating sarcopenia. Apelin also ameliorates muscle atrophy via PI3K/Akt, AMPK, and NF-κB pathways in skeletal muscle diseases including disuse muscle atrophy, metabolic muscle atrophy, and muscular dystrophy. This review aims to elaborate  on Apelin structure, distribution, and expression regulatory mechanisms in sarcopenia, clarify the pathways through which Apelin improves skeletal muscle function and mass, and provide theoretical support for targeted therapy.

Communication Author：WANG Hui-Guo , Email:wanghuiguo163@163.com ZHU Lin , Email:11251@gzsport.edu.cn LIU Xiao-Guang , Email:liuxg@gzsport.edu.cn