Neurohormonal factors in the development of catabolic/anabolic imbalance and cachexia

被引:35
作者
Brink, M
Anwar, A
Delafontaine, P
机构
[1] Fdn Rech Med, Div Cardiol, CH-1205 Geneva, Switzerland
[2] Univ Kansas, Med Ctr, Div Cardiovasc Dis, Kansas City, KS 66103 USA
关键词
congestive heart failure; angiotensin II; TNF-alpha; corticosterone; ubiquitin; insulin-like growth factor-I;
D O I
10.1016/S0167-5273(02)00239-5
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mechanisms that lead to cachexia are still poorly understood. The neurohormonal changes that occur in severe disease states may cause an imbalance between protein synthesis and degradation at the cellular level, followed by muscle wasting. Here, we review actions of angiotensin II, TNF-alpha, corticosteroids, insulin-like growth factor-I (IGF-I), and the IGF binding proteins, factors that may each contribute to the metabolic imbalance. The complex endocrine, autocrine and intracellular interactions between these factors will be described with examples from patient, rat and cell culture studies. Moreover, some of the data supporting that each of these hormones may directly affect cellular protein degradation mechanisms will be reviewed. Knowledge on these regulatory mechanisms will facilitate the development of new pharmaceutical strategies to treat cachexia. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:111 / 121
页数:11
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