Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA; MRC Cancer Unit, University of Cambridge, Hutchison Research Centre, Cambridge Biomedical Campus, Cambridge CB2 0XZ, UK.
Department of Nutritional Sciences, Rutgers School of Environmental and Biological Sciences, The State University of New Jersey, New Brunswick, NJ 08901, USA.
Cell. 2023 Apr 27;186(9):1824-1845. doi: 10.1016/j.cell.2023.03.028.
Cachexia, a systemic wasting condition, is considered a late consequence of diseases, including cancer, organ failure, or infections, and contributes to significant morbidity and mortality. The induction process and mechanistic progression of cachexia are incompletely understood. Refocusing academic efforts away from advanced cachexia to the etiology of cachexia may enable discoveries of new therapeutic approaches. Here, we review drivers, mechanisms, organismal predispositions, evidence for multi-organ interaction, model systems, clinical research, trials, and care provision from early onset to late cachexia. Evidence is emerging that distinct inflammatory, metabolic, and neuro-modulatory drivers can initiate processes that ultimately converge on advanced cachexia.
恶病质是一种全身性消耗状态,被认为是疾病的晚期后果,包括癌症、器官衰竭或感染,并导致发病率和死亡率显著增加。恶病质的诱导过程和机制进展尚不完全清楚。将学术研究的重点从晚期恶病质转移到恶病质的病因上,可能会发现新的治疗方法。在这里,我们回顾了从早期恶病质到晚期恶病质的驱动因素、机制、机体易感性、多器官相互作用的证据、模型系统、临床研究、试验和护理提供。有证据表明,不同的炎症、代谢和神经调节驱动因素可以启动最终导致晚期恶病质的过程。