期刊
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 121, 期 1-2, 页码 193-198出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2010.03.064
关键词
ADAM17; Kidney disease; Secondary hyperparathyroidism; Renoprotection
资金
- NIDDK NIH HHS [R01 DK062713, DK062713, R01 DK062713-04] Funding Source: Medline
In the course of kidney disease, the progressive loss of renal capacity to maintain normal serum levels of 1,25-dihydroxyvitamin D (1,25(OH)(2)D) is a main contributor to parathyroid hyperplasia and high serum PTH. High PTH causes mineral and skeletal abnormalities predisposing to ectopic calcifications and increased mortality. Intriguingly, replacement therapy with 1,25(OH)(2)D or its less calcemic analogs was recently shown to improve survival in kidney disease patients through renal and cardiovascular protective actions that are independent of PTH suppression. This work presents preliminary evidence that 1,25(OH)(2)D inhibition of TACE (Tumor necrosis factor Alpha Converting Enzyme) is a potential common mechanism underlying the efficacy of therapy with 1,25(OH)(2)D or its analogs to improve outcomes in chronic kidney disease. 1,25(OH)(2)D prevents/moderates not only the onset and progression of parathyroid TACE/TGF alpha-driven secondary hyperparathyroidism, but, more significantly, renal TACE/TGF alpha-driven fibrotic and inflammatory lesions to the renal parenchyma, and TACE/TNF alpha-driven systemic inflammation, which is known to aggravate renal and cardiovascular lesions and enhance the risk of vascular calcification and cardiovascular mortality. (C) 2010 Elsevier Ltd. All rights reserved.
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