Abstract：
Cachexia is a wasting syndrome that manifests in more than half of all cancer patients. Cancer-associated cachexia negatively influences the survival of patients and their quality of life. It is characterized by a rapid loss of adipose and skeletal muscle tissues, which is partly mediated by inflammatory cytokines. Here, we explored the crucial roles of interleukin-6 (IL-6) family cytokines, including IL-6, leukemia inhibitory factor, and oncostatin M, in the development of cancer cachexia. These cytokines have been shown to exacerbate cachexia by promoting the wasting of adipose and muscle tissues, activating mechanisms that enhance lipolysis and proteolysis. Overlapping effects of the IL-6 family cytokines depend on janus kinase/signal transducer and activator of transcription 3 signaling. We argue that the blockade of these cytokine pathways individually may fail due to redundancy and future therapeutic approaches should target common downstream elements to yield effective clinical outcomes.
摘要：
恶病质是一种消瘦综合征，在一半以上的癌症患者中表现出来。癌症相关恶病质对患者的生存和生活质量有负面影响。它的特点是脂肪和骨骼肌组织的快速损失，部分是由炎症细胞因子介导的。这里,我们探讨了白细胞介素-6（IL-6）家族细胞因子的关键作用，包括IL-6，白血病抑制因子，和制瘤素M，在癌症恶病质的发展中。这些细胞因子已被证明通过促进脂肪和肌肉组织的消耗而加剧恶病质，增强脂解和蛋白水解的激活机制。IL-6家族细胞因子的重叠作用取决于janus激酶/信号转导子和转录激活因子3信号传导。我们认为，由于冗余，单独阻断这些细胞因子途径可能会失败，未来的治疗方法应针对共同的下游元件，以产生有效的临床结果。
