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TGF-Beta Signaling in Bone with Chronic Kidney Disease
被引:15
作者:
Iwasaki, Yoshiko
[1
,3
]
Yamato, Hideyuki
[2
,4
]
Fukagawa, Masafumi
[2
,4
]
机构:
[1] Oita Univ Nursing & Hlth Sci, Dept Hlth Sci, Oita 8701163, Japan
[2] Tokai Univ Sch Med, Div Nephrol & Metab, Kanagawa 259119, Japan
[3] Oita Univ Nursing & Hlth Sci, Dept Hlth Sci, Oita 8701163, Japan
[4] Tokai Univ, Sch Med, Div Nephrol & Metab, Isehara, Kanagawa 259119, Japan
关键词:
bone remodeling;
mineral metabolism disturbance;
chronic kidney disease;
humoral factors;
GROWTH-FACTOR-BETA;
PATIENTS RECEIVING HEMODIALYSIS;
MESSENGER-RNA LEVELS;
PARATHYROID-HORMONE;
OSTEOCLAST DIFFERENTIATION;
OSTEOBLAST DIFFERENTIATION;
ALKALINE-PHOSPHATASE;
SKELETAL RESISTANCE;
CALCEMIC RESPONSE;
BINDING-PROTEIN;
D O I:
10.3390/ijms19082352
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Transforming growth factor (TGF)- 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- 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- is involved in the production and functions of these factors in bone. TGF- may act as a factor that mediates abnormal bone remodeling in CKD.
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页数:17
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