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Effects of GH/IGF axis on bone and cartilage

Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of the hypothalamic/pituitary somatotrophic axis t...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2021-01, Vol.519, p.111052-111052, Article 111052
Main Authors: Dixit, Manisha, Poudel, Sher Bahadur, Yakar, Shoshana
Format: Article
Language:English
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Summary:Growth hormone (GH) and its mediator, the insulin-like growth factor-1 (IGF-1) regulate somatic growth, metabolism and many aspects of aging. As such, actions of GH/IGF have been studied in many tissues and organs over decades. GH and IGF-1 are part of the hypothalamic/pituitary somatotrophic axis that consists of many other regulatory hormones, receptors, binding proteins, and proteases. In humans, GH/IGF actions peak during pubertal growth and regulate skeletal acquisition through stimulation of extracellular matrix production and increases in bone mineral density. During aging the activity of these hormones declines, a state called somatopaguss, which associates with deleterious effects on the musculoskeletal system. In this review, we will focus on GH/IGF-1 action in bone and cartilage. We will cover many studies that have utilized congenital ablation or overexpression of members of this axis, as well as cell-specific gene-targeting approaches used to unravel the nature of the GH/IGF-1 actions in the skeleton in vivo. •GH/IGF axis plays central roles in skeletal growth and mineral acquisition.•Cells of the osseous system express the GHR and the IGF-1R and secrete IGF-1 that acts in an autocrine/paracrine fashion.•GH/IGF stimulate proliferation and differentiation of chondrocytes in the growth plate, thus mediating linear bone growth.•IGF-1 enhances OB differentiation, collagen secretion, and bone matrix mineralization.•IGF-1 couples OB-induced bone formation and OCL-mediated bone resorption via activation of the ephrinB2/Eph4 system.
ISSN:0303-7207
1872-8057
1872-8057
DOI:10.1016/j.mce.2020.111052