TGF-Beta Signaling in Bone with Chronic Kidney Disease

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chronic kidney disease 4 nephrologydiseases
renal osteodystrophy 3 nephrologydiseases

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chronic kidney disease 905 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
chronic kidney disease 3870 and discuss the potential involvement of TGF-β action in the pathogenesis of bone abnormalities in chronic kidney disease (CKD).2. TGF-β Exists in Bone Tissue and Is Implicated in Bone MetabolismIn mammals, the TGF-β family
chronic kidney disease 32530 TGF-β in CKD-MBD.Figure 1Possible factors and pathways associated with the involvement of TGF-β in chronic kidney disease -mineral and bone disorder. Increasing TGF-β levels accompanied by renal dysfunction induces mineral
chronic kidney disease 32932 phenomena. Blue-shaded boxes indicate decreased levels of factors. Red X indicates regulatory disturbance in chronic kidney disease . T bar indicates inhibitory action of humoral factor. FGF23, fibroblast growth factor 23; PTH, parathyroid
renal osteodystrophy 13253 and bone metabolism are common complications in CKD. These abnormalities were traditionally termed renal osteodystrophy (ROD), and have been renamed “Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)” [[62]].Along
renal osteodystrophy 28967 osteochondrogenic transdifferentiation of vascular smooth muscle cells, vascular calcification, and renal osteodystrophy . However, elevated Dkk1 levels and downregulation of vascular klotho (both key findings in the abovementioned
renal osteodystrophy 30870 hypertrophy in an Alport syndrome model [[145]]. Thus, ActRIIA signaling may be the key factor that induces renal osteodystrophy , cardiovascular disease, and renal fibrosis.5. ConclusionsIn Figure 1, we summarize the possible involvement

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