Abstract
Transforming growth factor (TGF)-β signaling is not only important in skeletal development, but also essential in bone remodeling in adult bone. The bone remodeling process involves integrated cell activities induced by multiple stimuli to balance bone resorption and bone formation. TGF-β plays a role in bone remodeling by coordinating cell activities to maintain bone homeostasis. However, mineral metabolism disturbance in chronic kidney disease (CKD) results in abnormal bone remodeling, which leads to ectopic calcification in CKD. High circulating levels of humoral factors such as parathyroid hormone, fibroblast growth factor 23, and Wnt inhibitors modulate bone remodeling in CKD. Several reports have revealed that TGF-β is involved in the production and functions of these factors in bone. TGF-β may act as a factor that mediates abnormal bone remodeling in CKD.
Highlights
Transforming growth factor (TGF)-β superfamily molecules play critical roles in tissue development and differentiation in an autocrine/paracrine/endocrine manner [1]
We focus on the effect of TGF-β on bone remodeling and discuss the potential involvement of TGF-β action in the pathogenesis of bone abnormalities in chronic kidney disease (CKD)
The latent TGF-β binding protein (LTBP) binds with latent TGF-β to form a complex, which is secreted from osteoblastic cells
Summary
Transforming growth factor (TGF)-β superfamily molecules play critical roles in tissue development and differentiation in an autocrine/paracrine/endocrine manner [1]. Intramembranous ossification and endochondral ossification are skeletal ossification processes that take place following condensation of mesenchymal stem cells in fetal skeletal development [4,5]. During the endochondral ossification process, mesenchymal cells undergo chondrogenesis to form cartilage, which is later replaced by mineralized bone. TGF-β2-null mice display severe skeletal abnormalities in both intramembranous and endochondral ossification [8]. The skeleton in adults undergoes continuous renewal throughout life to maintain bone mass and bone strength to resist fracture. This process is critically dependent on the activities of two cell types and their interactions. Osteoblasts, which are derived from mesenchymal cells, deposit new bone matrix in the resorbed area and facilitate mineralization. We focus on the effect of TGF-β on bone remodeling and discuss the potential involvement of TGF-β action in the pathogenesis of bone abnormalities in chronic kidney disease (CKD)
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