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• W2017254352 abstract "The prevention or attenuation of disease-related skeletal muscle degeneration has been a common goal in the treatment of cardiac cachexia. Cell-based therapies are complicated by insufficient numbers of autologous myoblasts and by ineffective incorporation into host muscle. Pharmacological administration of growth hormone in a variety of clinical conditions characterized by an increase in catabolic rate have been associated with increases in mortality and morbidity, resulting in a decrease in the clinical use of growth hormone and its downstream effector, insulin-like growth factor-1 and a decline in general research into anabolic treatment strategies. In mouse models, however, the selective expression of a muscle-specific transgene encoding a locally acting IGF-1 isoform induces muscle hypertrophy, prevents age- or disease-related atrophy, by increasing stem cell recruitment to injured or degenerating tissue. This gene-based approach avoids hypertrophic effects on distal organs such as the heart, and eliminates risk of possible neoplasms induced by inappropriate high expression levels of circulating IGF-1. The potential therapeutic role of locally expressed IGF-1 is discussed in the context of current strategies for the attenuation of cardiac cachexia." @default.
• W2017254352 created "2016-06-24" @default.
• W2017254352 creator A5037361891 @default.
• W2017254352 creator A5042049867 @default.
• W2017254352 date "2002-09-01" @default.
• W2017254352 modified "2023-09-27" @default.
• W2017254352 title "Gene therapy for cardiac cachexia?" @default.
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• W2017254352 doi "https://doi.org/10.1016/s0167-5273(02)00253-x" @default.
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