Abstract: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.