Endogenous Glucocorticoid Metabolism in Bone: Friend or Foe

被引：11

作者：

Martin, Claire S. ^{[1
]}

Cooper, Mark S. ^{[2
]}

Hardy, Rowan S. ^{[3
,4
]}

机构：

[1] Univ Birmingham, Inst Metab & Syst Res, Birmingham, W Midlands, England

[2] Univ Sydney, Australian & New Zealand Army Corps ANZAC Res Ins, Sydney, NSW, Australia

[3] Univ Birmingham, Birmingham, W Midlands, England

[4] Univ Birmingham, Inst Clin Sci, Birmingham, W Midlands, England

来源：

FRONTIERS IN ENDOCRINOLOGY | 2021年 / 12卷

基金：

英国惠康基金;

关键词：

glucocorticoid; bone; 11beta-hydroxysteroid dehydrogenase; osteoclast; osteoblast; osteoporosis; chronic inflammation; 11-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE-1; ENDOTHELIAL-GROWTH-FACTOR; CORTICOSTEROID-BINDING GLOBULIN; LOW-DOSE PREDNISONE; RHEUMATOID-ARTHRITIS; OSTEOBLAST DIFFERENTIATION; MINERAL DENSITY; SYNTHETIC MINERALOCORTICOIDS; INFLAMMATORY MARKERS; REPLACEMENT THERAPY;

D O I：

10.3389/fendo.2021.733611

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The role of tissue specific metabolism of endogenous glucocorticoids (GCs) in the pathogenesis of human disease has been a field of intense interest over the last 20 years, fuelling clinical trials of metabolism inhibitors in the treatment of an array of metabolic diseases. Localised pre-receptor metabolism of endogenous and therapeutic GCs by the 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) enzymes (which interconvert endogenous GCs between their inactive and active forms) are increasingly recognised as being critical in mediating both their positive and negative actions on bone homeostasis. In this review we explore the roles of endogenous and therapeutic GC metabolism by the 11 beta-HSD enzymes in the context of bone metabolism and bone cell function, and consider future strategies aimed at modulating this system in order to manage and treat various bone diseases.

引用

页数：13

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