Does osteocytic SOST suppression mediate PTH bone anabolism?

被引：95

作者：

Kramer, Ina ^{[1
]}

Keller, Hansjoerg ^{[1
]}

Leupin, Olivier ^{[1
]}

Kneissel, Michaela ^{[1
]}

机构：

[1] Novartis Inst BioMed Res, Musculoskeletal Dis Area, CH-4002 Basel, Switzerland

来源：

TRENDS IN ENDOCRINOLOGY AND METABOLISM | 2010年 / 21卷 / 04期

关键词：

INTERMITTENT PARATHYROID-HORMONE; WNT SIGNALING PATHWAY; GENE-EXPRESSION; POSTMENOPAUSAL OSTEOPOROSIS; TRANSCRIPTION FACTORS; TRABECULAR BONE; LRP5; MUTATIONS; MESSENGER-RNA; CORTICAL BONE; HIP FRACTURE;

D O I：

10.1016/j.tem.2009.12.002

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Parathyroid hormone (PIN) has bone anabolic activity when administered intermittently, affecting cells of the osteoblastic lineage at various stages, yet much remains to be learned about precisely how PTH promotes osteoblastic bone formation. Recent discoveries revealed that PTH causes transcriptional suppression of the osteocyte marker gene SOST, which encodes the potent secreted bone formation inhibitor, sclerostin. This review addresses whether osteocytes, terminally differentiated cells of the osteoblastic lineage, which are entrapped within the mineralized bone matrix, contribute to PTH-induced bone formation responses via regulation of sclerostin levels, and discusses recent evidence on how the bone anabolic responses elicited by intermittent PTH treatment or by sclerostin inhibition overlap and diverge.

引用

页码：237 / 244

页数：8

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