改善生存率和生活质量是肿瘤患者成功治疗的主要目标，恶液质治疗也是肿瘤治疗的重要部分之一。肿瘤恶液质是一组症状和体征，常见于晚期转移的肿瘤，恶液质可在50%的肿瘤患者中出现，是肿瘤患者死亡的主要原因之一。虽然恶液质的进展与肿瘤患者的发病率和死亡率直接相关，但是恶液质的发病机制和治疗仍然不清。有证据表明，肿瘤引起的体重减轻与全身内分泌和代谢异常以及许多组织和器官的功能破坏有关，其中肿瘤引起的骨骼肌消耗已成为重要的研究方向。近年来，肿瘤恶液质中骨骼肌氧化代谢调节作用得到越来越多的关注，氧化代谢已经成为肿瘤患者肌肉萎缩的生物学治疗靶点之一。虽然骨骼肌对炎症、激素和收缩等外界刺激的反应需要涉及多种细胞器对细胞信号通路的整合，但是肌肉线粒体参与调节消耗和代谢过程的作用已经得到确认，线粒体含量和功能受到机体许多刺激因素的影响，包括肌肉活动增加和减少，全身炎症和全身性激素信号传导等。随着恶液质进展，炎症细胞因子增加和性类固醇的降低可以破坏肌肉氧化代谢能力，恶液质患者活动力的下降与骨骼肌消耗萎缩密切相关。本篇综述将探讨与肿瘤恶液质相关的骨骼肌氧化代谢调节的作用及进展。

Abstract:Improving the survival rate and quality of life is the main goal for the successful treatment of cancer patients. Treatment of cachexia is also an important part of cancer treatment. Cancer cachexia is a group of symptoms and signs commonly seen in advanced metastatic tumors. Cachexia may occur in 50% of cancer patients and is one of the leading causes of cancer death.Although the progression of cachexia is directly related to the morbidity and mortality of cancer patients, the pathogenesis and treatment of cachexia are still unclear. There is evidence that cancer-induced weight loss is associated with global endocrine and metabolic abnormalities, and the disrupted function of many tissues and organs. Skeletal muscle consumption caused by cancer has become an important research direction. In recent years, more attention has been paid to the regulation of skeletal muscle oxidative metabolism in cancer cachexia. Oxidative metabolism has become one of the biological therapeutic targets for cancer muscle atrophy.The response of skeletal muscle to external stimuli such as inflammation, hormones, and contraction requires integrated cellular signaling pathways involving several organelles and structures. Although the response of skeletal muscle to external stimuli such as inflammation, hormones, and contraction requires integrated cellular signaling pathways involving several organelles and structures, the involvement of muscle mitochondria in the regulation of both wasting and metabolic quality has become firmly established. Mitochondrial content and function are altered by a host of stimuli, including increased and decreased use, systemic inflammation, and systemic hormonal signaling. With the development of cachexia, the increase of inflammatory cytokines and the decrease of steroids can destroy the ability of muscle oxidative metabolism. The decrease of activity in cachexia patients is closely related to the atrophy of skeletal muscle consumption. In this review, we will explore the role and progression of skeletal muscle oxidative metabolism regulation related to cancer cachexia.