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骨骼与肾脏:肾性骨营养不良分子机制的系统生物学研究方法

Bone and the kidney: a systems biology approach to the molecular mechanisms of renal osteodystrophy.

作者信息

Mondry Adrian, Wang Zhengyuan, Dhar Pawan K

机构信息

Bioinformatics Institute, Singapore.

出版信息

Curr Mol Med. 2005 Aug;5(5):489-96. doi: 10.2174/1566524054553531.

DOI:10.2174/1566524054553531
PMID:16101478
Abstract

Despite its apparent static condition, the skeleton undergoes a permanent process of remodeling mediated by osteoblasts and osteoclasts. The activity of these cells is regulated by a plethora of factors, ranging from mechanical stress to the effects of hormones to the immune system. One well-studied regulatory system involves the maintenance of calcium homeostasis through a network whose main regulatory components include ionized calcium, phosphate, parathyroid hormone and active vitamin D. This system establishes the link between bone and kidney, as one of the kidney's endocrine functions is the activation of vitamin D, while electrolyte homeostasis is one of its excretory functions. Impaired renal function leads to disturbances in this regulatory system, resulting in the complex syndrome of renal osteodystrophy that affects the majority of patients with chronic renal failure. This review summarizes the current understanding of bone physiology on a molecular level, examines some of the pathological pathways related to renal disease, and concludes with an outlook on how the emerging field of systems biology may contribute to a more dynamic and quantitative understanding of the physiology and pathophysiology of renal bone disease.

摘要

尽管骨骼表面看似处于静止状态,但它却经历着由成骨细胞和破骨细胞介导的持续重塑过程。这些细胞的活性受众多因素调节,从机械应力到激素作用再到免疫系统。一个经过充分研究的调节系统涉及通过一个网络维持钙稳态,该网络的主要调节成分包括离子钙、磷酸盐、甲状旁腺激素和活性维生素D。这个系统建立了骨骼与肾脏之间的联系,因为肾脏的内分泌功能之一是激活维生素D,而电解质稳态是其排泄功能之一。肾功能受损会导致这个调节系统紊乱,从而引发影响大多数慢性肾衰竭患者的复杂肾性骨营养不良综合征。本综述总结了目前在分子水平上对骨生理学的理解,探讨了一些与肾脏疾病相关的病理途径,并展望了新兴的系统生物学领域如何有助于更动态、定量地理解肾性骨病的生理学和病理生理学。

相似文献

1
Bone and the kidney: a systems biology approach to the molecular mechanisms of renal osteodystrophy.骨骼与肾脏:肾性骨营养不良分子机制的系统生物学研究方法
Curr Mol Med. 2005 Aug;5(5):489-96. doi: 10.2174/1566524054553531.
2
The role of phosphate and other factors on the pathogenesis of renal osteodystrophy.磷酸盐及其他因素在肾性骨营养不良发病机制中的作用。
Adv Exp Med Biol. 1977;81:467-75. doi: 10.1007/978-1-4613-4217-5_47.
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Renal osteodystrophy in children: the role of vitamin D, phosphorus, and parathyroid hormone.儿童肾性骨营养不良:维生素D、磷和甲状旁腺激素的作用
Am J Kidney Dis. 1986 Apr;7(4):275-84. doi: 10.1016/s0272-6386(86)80068-3.
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Renal osteodystrophy in children: pathogenesis, diagnosis and treatment.儿童肾性骨营养不良:发病机制、诊断与治疗
Curr Opin Pediatr. 2014 Apr;26(2):180-6. doi: 10.1097/MOP.0000000000000061.
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Systemic Activation of Activin A Signaling Causes Chronic Kidney Disease-Mineral Bone Disorder.激活素 A 信号的系统激活导致慢性肾脏病-矿物质骨代谢紊乱。
Int J Mol Sci. 2018 Aug 23;19(9):2490. doi: 10.3390/ijms19092490.
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[Renal osteodystrophy-II-Recent therapeutic acquisitions (author's transl)].肾性骨营养不良-II-近期治疗进展(作者译)
Nouv Presse Med. 1977 Nov 12;6(38):3533-7.
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Renal osteodystrophy.肾性骨营养不良
Baillieres Clin Endocrinol Metab. 1988 Feb;2(1):193-241. doi: 10.1016/s0950-351x(88)80013-2.
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Adynamic bone and chronic renal failure: an overview.动力缺失性骨病与慢性肾衰竭:概述
Am J Med Sci. 2000 Aug;320(2):81-4. doi: 10.1097/00000441-200008000-00003.
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Renal osteodystrophy.肾性骨营养不良
Orthop Clin North Am. 1984 Oct;15(4):687-95.
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Evolution of renal osteodystrophy: correlation of bone histomorphometry and serum mineral and immunoreactive parathyroid hormone values before and after treatment with calcium carbonate or 25-hydroxycholecalciferol.肾性骨营养不良的演变:碳酸钙或25-羟胆钙化醇治疗前后骨组织形态计量学与血清矿物质及免疫反应性甲状旁腺激素值的相关性
Kidney Int Suppl. 1975 Jan(2):102-12.

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