Neural Mechanisms of Cancer Cachexia.
Neural Mechanisms of Cancer Cachexia.
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DOI：
10.3390/cancers13163990
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发表时间：
2021-08-07
期刊：
影响因子：
5.2
通讯作者：
Marks DL
中科院分区：
文献类型：
--
作者：
Olson B;Diba P;Korzun T;Marks DL
癌症恶病质是一种毁灭性的消耗综合征，发生在许多疾病中，其体征和症状包括厌食症、体重减轻、认知障碍和疲劳。大脑能够对全身代谢施加全面的稳态控制，并且越来越被认为是癌症恶病质的重要介质。鉴于对癌症恶病质神经机制的认识和发现不断增加，我们试图对大脑启动和传播癌症恶病质程序的机制进行深入的回顾和更新。此外，最近的工作已经确定了恶病质的新分子介质，通过与大脑的直接相互作用发挥其作用。因此，本文将对恶病质的神经机制进行综述，并对最近发现的癌症恶病质的神经介质进行讨论。近一半的癌症患者患有恶病质，这是一种代谢综合征，以脂肪和瘦肉质量的进行性萎缩为特征。这种过度分解代谢的状态会降低生活质量、耐受治疗的能力和最终的生存率，但目前还没有有效的治疗方法。虽然中枢神经系统（CNS）协调了恶病质的几种表现，但在恶病质期间神经功能障碍的确切机制仍未揭示。在此，我们总结了癌症恶病质期间中枢神经系统功能障碍的细胞和分子机制，重点关注炎症、自主神经和神经内分泌过程，最后讨论了最近发现的中枢神经系统恶病质介质，包括GDF15、LCN2和INSL3。
Cancer cachexia is a devastating wasting syndrome that occurs in many illnesses, with signs and symptoms including anorexia, weight loss, cognitive impairment and fatigue. The brain is capable of exerting overarching homeostatic control of whole-body metabolism and is increasingly being recognized as an important mediator of cancer cachexia. Given the increased recognition and discovery of neural mechanisms of cancer cachexia, we sought to provide an in-depth review and update of mechanisms by which the brain initiates and propagates cancer cachexia programs. Furthermore, recent work has identified new molecular mediators of cachexia that exert their effects through their direct interaction with the brain. Therefore, this review will summarize neural mechanisms of cachexia and discuss recently identified neural mediators of cancer cachexia. Nearly half of cancer patients suffer from cachexia, a metabolic syndrome characterized by progressive atrophy of fat and lean body mass. This state of excess catabolism decreases quality of life, ability to tolerate treatment and eventual survival, yet no effective therapies exist. Although the central nervous system (CNS) orchestrates several manifestations of cachexia, the precise mechanisms of neural dysfunction during cachexia are still being unveiled. Herein, we summarize the cellular and molecular mechanisms of CNS dysfunction during cancer cachexia with a focus on inflammatory, autonomic and neuroendocrine processes and end with a discussion of recently identified CNS mediators of cachexia, including GDF15, LCN2 and INSL3.
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DOI：
10.1084/jem.20111020
发表时间：
2011-11-21
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Braun TP;Zhu X;Szumowski M;Scott GD;Grossberg AJ;Levasseur PR;Graham K;Khan S;Damaraju S;Colmers WF;Baracos VE;Marks DL
通讯作者：
Marks DL
DOI：
10.1016/j.bbi.2018.05.021
发表时间：
2018-10
期刊：
Brain, behavior, and immunity
影响因子：
--
作者：
Burfeind KG;Zhu X;Levasseur PR;Michaelis KA;Norgard MA;Marks DL
通讯作者：
Marks DL
影响因子：
4.8
作者：
BERNARDINI, R;KAMILARIS, TC;CHROUSOS, GP
通讯作者：
CHROUSOS, GP
影响因子：
11.1
作者：
Balusu S;Van Wonterghem E;De Rycke R;Raemdonck K;Stremersch S;Gevaert K;Brkic M;Demeestere D;Vanhooren V;Hendrix A;Libert C;Vandenbroucke RE
通讯作者：
Vandenbroucke RE
影响因子：
7.3
作者：
Burfeind KG;Michaelis KA;Marks DL
通讯作者：
Marks DL