IGF-1 Pathways refer to the complex cascade of molecular signaling initiated by Insulin-like Growth Factor 1, a polypeptide hormone structurally similar to insulin that plays a pivotal role in cell proliferation, differentiation, and survival across various tissues. In the context of hormonal health, IGF-1 acts as a primary mediator of Growth Hormone (GH) action, predominantly synthesized in the liver but also locally in target tissues like muscle and bone. This signaling network is central to somatic growth during development and, in adulthood, to metabolic regulation, tissue repair, and the overall physiology of aging. Dysregulation of these pathways is implicated in both growth disorders and conditions related to accelerated cellular senescence.
Origin
The term is rooted in the discovery of a factor mediating the growth-promoting effects of Growth Hormone, initially termed “sulfation factor” and later identified as Insulin-like Growth Factor 1. The concept of “pathways” stems from molecular biology, describing the sequence of biochemical reactions and protein interactions that transmit a signal from the cell surface receptor to the nucleus. The clinical relevance of IGF-1 pathways solidified as its role in metabolic health, longevity, and oncogenesis became clearer through extensive endocrinology research.
Mechanism
The signaling mechanism begins when circulating IGF-1 binds to the IGF-1 receptor (IGF-1R) on the cell surface, which is a receptor tyrosine kinase. This binding triggers the autophosphorylation of the receptor, initiating an intracellular cascade, primarily through the PI3K/Akt and MAPK signaling pathways. Activation of the PI3K/Akt pathway is critical for promoting cellular survival and inhibiting apoptosis, while the MAPK pathway typically drives cell proliferation. The overall effect is a potent anabolic signal that regulates protein synthesis, glucose metabolism, and cellular growth across the body.
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