Effects of GH/IGF axis on bone and cartilage
Manisha Dixit Molecular and Cellular Endocrinology Volume 519, 1 January 2021, 111052
Highlights
• 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.
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.