Kong Jianda, Xie Yingao, Fan Rao, Wang Qinglu, Luo Ying, Dong Panpan
College of Basic Medicine, Qilu Medical University, Zibo, China.
School of Physical Education, Qufu Normal University, Qufu, China.
Eur J Med Res. 2025 Jun 12;30(1):475. doi: 10.1186/s40001-025-02751-9.
Aging is a systemic process marked by progressive multi-organ dysfunction, metabolic dysregulation, and chronic low-grade inflammation ("inflammaging"), which collectively drive neurodegenerative diseases such as Alzheimer's Disease (AD) and Parkinson's Disease (PD). Emerging evidence underscores the brain-muscle-liver axis as a central hub for maintaining energy homeostasis and neuroimmune crosstalk during aging. Here, we elucidate how exercise orchestrates inter-organ communication to counteract age-related decline through metabolic reprogramming, immunomodulation, and neuroprotection. Mechanistically, exercise enhances mitochondrial biogenesis and oxidative capacity in skeletal muscle via AMPK/PGC-1α signaling, restoring fatty acid oxidation and glucose metabolism while producing myokines (e.g., BDNF and IL-6) that promote neuronal survival and synaptic plasticity. Concurrently, hepatic SIRT1 activation promotes lipid metabolism, mitigates insulin resistance, and reduces systemic inflammation, hence preserving brain energy supply. In the aging brain, exercise stimulates neurogenesis, suppresses neuroinflammation via NF-κB inhibition, and elevates BDNF levels, which synergistically enhance cognitive resilience. vitally, exercise modulates the neuro-immunometabolic axis by balancing pro- and anti-inflammatory cytokines (e.g., IL-6's hormetic role), optimizing immune cell function, and enhancing autophagy-mediated clearance of toxic aggregates (Aβ, α-synuclein). These adaptations are further amplified by epigenetic reprogramming, including but not limited to Nrf2-driven antioxidant responses and circadian rhythm synchronization. Our synthesis highlights exercise as a pleiotropic intervention that transcends single-organ influences, instead leveraging multi-tissue networks to delay aging and neurodegeneration. Unresolved challenges-personalized exercise regimens, molecular biomarkers for efficacy prediction, and combinatorial therapies with pharmacologic agents-underscore the need for translational studies integrating omics technologies and circadian biology. By bridging mechanistic insights with clinical applications, this review positions exercise as a cornerstone of precision medicine for aging populations.
衰老 是一个系统性过程,其特征为进行性多器官功能障碍、代谢失调和慢性低度炎症(“炎症衰老”),这些因素共同驱动神经退行性疾病,如阿尔茨海默病(AD)和帕金森病(PD)。新出现的证据强调,脑-肌肉-肝脏轴是衰老过程中维持能量稳态和神经免疫串扰的核心枢纽。在这里,我们阐明运动如何通过代谢重编程、免疫调节和神经保护来协调器官间的通讯,以对抗与年龄相关的衰退。从机制上讲,运动通过AMPK/PGC-1α信号通路增强骨骼肌中的线粒体生物发生和氧化能力,恢复脂肪酸氧化和葡萄糖代谢,同时产生促进神经元存活和突触可塑性的肌动蛋白(如脑源性神经营养因子和白细胞介素-6)。同时,肝脏中SIRT1的激活促进脂质代谢,减轻胰岛素抵抗,并减少全身炎症,从而维持大脑能量供应。在衰老的大脑中,运动刺激神经发生,通过抑制NF-κB抑制神经炎症,并提高脑源性神经营养因子水平,这些协同增强认知恢复力。至关重要的是,运动通过平衡促炎和抗炎细胞因子(如白细胞介素-6的 hormetic 作用)、优化免疫细胞功能以及增强自噬介导的有毒聚集体(Aβ、α-突触核蛋白)清除来调节神经免疫代谢轴。这些适应性变化通过表观遗传重编程进一步放大,包括但不限于Nrf2驱动的抗氧化反应和昼夜节律同步。我们的综述强调运动是一种多效性干预措施,它超越了单一器官的影响,而是利用多组织网络来延缓衰老和神经退行性变。尚未解决的挑战——个性化运动方案、用于疗效预测的分子生物标志物以及与药物的联合治疗——强调了整合组学技术和昼夜生物学的转化研究的必要性。通过将机制性见解与临床应用相结合,本综述将运动定位为老年人群精准医学的基石。