Department of Health and Human Physiology, and the Holden Comprehensive Cancer Center, University Iowa, Iowa City, IA 52242, USA.
Department of Pediatrics, Darby Children's Research Institute, and the Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
Trends Cancer. 2022 May;8(5):397-403. doi: 10.1016/j.trecan.2022.01.004. Epub 2022 Feb 18.
The cachexia syndrome in cancer is characterized by weight loss resulting from the combination of anorexia and atrophy of adipose and skeletal muscle. For decades, inflammatory circulatory factors have been identified to regulate wasting, but inhibitors of these factors have not yielded the same clinical benefit as in animal models. Therefore, additional mediators of cachexia likely regulate this syndrome, and such factors might be more suitable for targeted intervention. We highlight several anorexia-cachexia signaling mediators, including activin A, myostatin, GDF15, and lipocalin-2. We discuss current evidence that these factors associate with cachexia in cancer patients, and summarize translational efforts including essential early-phase clinical trials. We conclude with thoughts on targeted and personalized approaches for future anti-cachexia treatments.
癌症恶病质综合征的特征是体重下降，这是厌食和脂肪及骨骼肌萎缩共同作用的结果。几十年来，人们已经确定了炎症循环因子来调节消耗，但这些因子的抑制剂并未产生与动物模型相同的临床获益。因此，恶病质的其他介质可能调节该综合征，并且这些因子可能更适合于靶向干预。我们强调了几种厌食-恶病质信号转导介质，包括激活素 A、肌肉生长抑制素、GDF15 和脂联素-2。我们讨论了这些因子与癌症患者恶病质相关的现有证据，并总结了包括关键性早期临床试验在内的转化研究。最后，我们对未来抗恶病质治疗的靶向和个性化方法进行了思考。
