科研之友
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摘要
Cancer cachexia is a multifactorial syndrome characterized by an ongoing loss of skeletal muscle mass, which negatively affects quality of life and portends a poor prognosis. Numerous molecular substrates and mechanisms underlie the dys-regulation of skeletal muscle synthesis and degradation observed in cancer cachexia, including proinflammatory cytokines (TNF alpha, IL1, and IL6), and the NF-kappa B, IGF1/AKT/mTOR, and myostatin/activin-SMAD pathways. Recent pre-clinical and clinical studies have demonstrated that anti-cachexia drugs (such as MABp1 and soluble receptor antagonist of myostatin/activin) not only prevent muscle wasting but also may prolong overall survival. In this review, we focus on the significance of cachexia signaling in patients with cancer and highlight promising drugs targeting tumor cachexia in clinical development.
- 出版日期2016-8-15
