Abstract
Aging is a complex biological process, which determines the life span of an organism. Insulin-like growth factor (IGF) and Wnt signaling pathways govern the process of aging. Both pathways share common downstream targets that allow competitive crosstalk between these branches. Of note, a shift from IGF to Wnt signaling has been observed during aging of satellite cells. Biological regulatory networks necessary to recreate aging have not yet been discovered. Here, we established a mathematical in silico model that robustly recapitulates the crosstalk between IGF and Wnt signaling. Strikingly, it predicts critical nodes following a shift from IGF to Wnt signaling. These findings indicate that this shift might cause age-related diseases.
Highlights
Aging is a highly complex biological process, which impacts health-related quality of life and life expectancy
We created a model of the molecular interactions between Insulin-like growth factor (IGF) and Wnt signaling in satellite cells and muscle aging by integrating more than 80 publications of the IGF/Wnt research field
Knowledge concerning the interaction of IGF and Wnt signaling as a whole is still missing
Summary
Aging is a highly complex biological process, which impacts health-related quality of life and life expectancy. The underlying mechanisms of aging are still poorly understood. Several theories have been postulated concerning the cause of aging. On a cellular level aging is, for instance, provoked by DNA damage, protein aggregation or cellular dysdifferentiation [1,2,3,4,5]. As a consequence, aging is commonly accompanied by a plethora of aging-related diseases such as cancer, neurodegenerative diseases, diabetes, osteoporosis and cardiovascular diseases [6]. A better understanding of the underlying pathways regulating life span serves as a basis to establish age-related therapy concepts
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