Cachexia is characterized by body weight loss due to extensive skeletal muscle wasting with or without adipose tissue loss. Many cancer patients experience cachexia symptoms which contribute to poor quality of life and increased mortality. However, there is currently no approved treatment that can effectively counteract cancer cachexia. In addition, the mechanisms underlying global muscle loss in the setting of cancer are poorly understood, thus representing a major challenge for the development of new therapies. While prior studies have focused on the role of inflammatory cytokines that can directly reduce muscle survival and function, less is known about the potential role of muscle vascular dysfunction as a mediator of cancer cachexia. Thus, my research interesting is to understand the molecular mediators involved in endothelial function and muscle maintenance which could have a significant impact on developing novel therapies to prevent cancer cachexia.