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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Published in | Molecular and cellular endocrinology Vol. 519; p. 111052 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
Ireland
Elsevier B.V
01.01.2021
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Subjects | |
Online Access | Get full text |
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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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Equally contributed to the review. |
ISSN: | 0303-7207 1872-8057 1872-8057 |
DOI: | 10.1016/j.mce.2020.111052 |