Key result
Growth hormone regulates post-natal mammalian growth indirectly through IGF-I production mediated by the JAK2/STAT5b signaling pathway, alongside other pathways critical for metabolic actions.
This review summarizes the mechanisms of the growth hormone cascade, highlighting the role of the JAK2/STAT5b pathway in IGF-I production and skeletal growth.
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Informs pediatric growth disorder evaluation; leaves open targeted JAK2/STAT5b therapies pending trials.
The myriad actions of growth hormone (GH) are still incompletely understood, despite decades of research. Although it is a major regulator of post-natal growth in mammals, much of its effects on skeletal growth are recognized to be mediated indirectly, through the stimulation of production of insulin-like growth factor (IGF)-I, as well as some of the major serum carrier proteins for IGF-I and -II, such as IGF-binding protein-3 (IGFBP-3) and the acid-labile subunit (ALS). The regulation of IGF-I production by GH appears to be mediated entirely by signalling through the Janus kinase (JAK) 2 pathway, via the phosphorylation of the transcription factor, signal transducer and activator of transcription (STAT) 5b. GH also signals, however, through additional pathways that are likely to be critical to the metabolic actions of GH.
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Rosenfeld et al. (2009) reported a review. Growth hormone was evaluated. Growth hormone regulates post-natal mammalian growth indirectly through IGF-I production mediated by the JAK2/STAT5b signaling pathway, alongside other pathways critical for metabolic actions.
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