Insulin-like growth factor-1 and muscle wasting in chronic heart failure

2005 ◽  
Vol 37 (10) ◽  
pp. 2023-2035 ◽  
Author(s):  
P. Christian Schulze ◽  
Ulrike Späte
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Chronic Heart Failure ◽  
Muscle Wasting ◽  
Insulin Like Growth Factor

Plasma insulin-like growth factor I as predictor of progression and all cause mortality in chronic heart failure

2009 ◽  
Vol 19 (6) ◽  
pp. 486-490 ◽  
Author(s):  
Mikkel Andreassen ◽  
Caroline Kistorp ◽  
Ilan Raymond ◽  
Per Hildebrandt ◽  
Finn Gustafsson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Growth Factor ◽  
Chronic Heart Failure ◽  
Plasma Insulin ◽  
Insulin Like Growth Factor ◽  
Factor I ◽  
All Cause Mortality ◽  
Growth Factor I

scholarly journals The mechanisms of muscle wasting in COPD and heart failure

2012 ◽  
Author(s):  
Giorgio Vescovo
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Growth Hormone ◽  
Growth Factor ◽  
Ubiquitin Ligase ◽  
Muscle Wasting ◽  
The Body ◽  
Adrenergic System ◽  
Muscle Dysfunction ◽  
Insulin Like Growth Factor

Many of the mechanisms leading to skeletal muscle wasting in COPD and heart failure are common to both conditions. These encompass neurohormonal activation and systemic inflammation. The mechanisms leading to muscle dysfunction are both qualitative and quantitative. Qualitative changes comprise the transition from aerobic metabolism and prevalent slow fibers composition toward anaerobic metabolism and fast fibers synthesis. Quantitative changes are mainly linked to muscle loss. These changes occur not only in the major muscles bulks of the body but also in respiratory muscles. The mechanisms leading to muscle wastage include cytokine-triggered skeletal muscle apoptosis and ubiquitin-proteasomeand non-ubiquitin-dependent pathways. The regulation of fiber type involves the growth hormone/insulin-like growth factor 1/calcineurin/transcriptional coactivator PGC1 cascade. The imbalance between protein synthesis and degradation plays an important role. Protein degradation can occur through ubiquitin-dependent and non-ubiquitin-dependent pathways. Very recently, two systems controlling ubiquitin-proteasome activation have been described: FOXO-ubiquitin ligase and NFkB ubiquitin ligase. These are triggered by TNFα and growth hormone/insulin-like growth factor 1. Moreover, apoptosis, which is triggered by tumor necrosis factor α, plays an important role. Another mechanism acting on muscle wastage is malnutrition, with an imbalance between catabolic and anabolic factors toward the catabolic component. Catabolism is also worsened by the activation of the adrenergic system and alteration of the cortisol/DEHA ratio toward cortisol production. Sarcomeric protein oxidation and its consequent contractile impairment can be another cause of skeletal muscle dysfunction in CHF.

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