摘要
背景:肾脏疾病是一个严重影响人类健康的问题,但如何有效地治疗已建立的慢性肾脏病却缺乏重要的知识。不断增加的证据动物和临床研究表明,维生素D受体(VDR)激活对多种肾脏疾病有良好的治疗作用。 方法:对多种肾脏疾病(如IgA肾病、特发性肾病综合征、肾细胞癌)中VDR结构和功能的研究文献进行结构化检索。对多个数据库进行了Inoma、糖尿病肾病、狼疮肾炎和针对VDR的治疗。 结果:本研究包括177篇发表的研究成果。这些研究表明,VdR激活参与了肾损伤的保护作用。EY病的发病机制有多种,包括抑制RAS活化、抗炎、抑制肾纤维化形成、恢复线粒体功能、抑制自身免疫功能和人的免疫功能。AL细胞凋亡 结论:VDR是治疗肾脏疾病的理想靶点。增加我们对肾脏中vdr的理解是一个研究的沃土,并可能在战斗中提供有效的武器。对抗肾脏疾病。
关键词: 维生素D受体,肾损伤,肾小管上皮细胞,慢性肾脏疾病,肾性骨性营养不良,急性肾损伤。
Current Medicinal Chemistry
Title:Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases
Volume: 25 Issue: 27
关键词: 维生素D受体,肾损伤,肾小管上皮细胞,慢性肾脏疾病,肾性骨性营养不良,急性肾损伤。
摘要: Background: Kidney disease is a serious problem that adversely affects human health, but critical knowledge is lacking on how to effectively treat established chronic kidney disease. Mounting evidence from animal and clinical studies has suggested that Vitamin D Receptor (VDR) activation has beneficial effects on various renal diseases.
Methods: A structured search of published research literature regarding VDR structure and function, VDR in various renal diseases (e.g., IgA nephropathy, idiopathic nephrotic syndrome, renal cell carcinoma, diabetic nephropathy, lupus nephritis) and therapies targeting VDR was performed for several databases.
Result: Included in this study are the results from 177 published research articles. Evidence from these papers indicates that VDR activation is involved in the protection against renal injury in kidney diseases by a variety of mechanisms, including suppression of RAS activation, anti-inflammation, inhibiting renal fibrogenesis, restoring mitochondrial function, suppression of autoimmunity and renal cell apoptosis.
Conclusion: VDR offers an attractive druggable target for renal diseases. Increasing our understanding of VDR in the kidney is a fertile area of research and may provide effective weapons in the fight against kidney diseases.
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Cite this article as:
Vitamin D Receptor: A Novel Therapeutic Target for Kidney Diseases, Current Medicinal Chemistry 2018; 25 (27) . https://dx.doi.org/10.2174/0929867325666180214122352
DOI https://dx.doi.org/10.2174/0929867325666180214122352 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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