摘要
Fractalkine受体趋化因子(C-X3-C motif)受体1(CX3CR1)及其高选择性配体CX3CL1介导免疫细胞趋化和粘附,这些趋化因子与免疫细胞粘附有关。许多炎症性疾病和恶性肿瘤的进展。CX3CL1/CX3CR1轴最近成为潜在的治疗靶点,因为它参与了个体发育,同源性。抽动迁移,或肾吞噬细胞定植。我们进行了Medline/PubMed搜索,以检测最近发表的研究,这些研究探讨了CX3CL1/CX3CR1轴与肾脏di之间的关系。肾病和疾病,包括糖尿病肾病、同种异体肾排斥反应、感染性肾脏疾病、IgA肾病、纤维化肾病、狼疮肾炎和肾小球肾炎、急性肾损伤与肾癌。大多数研究表明其在促进肾致病作用;然而,最近的一些研究表明,CX3CL1 /也可以减少肾pathopoies CX3CR1轴是.因此,CX3CL1/CX3CR1轴现在被认为是一把双刃剑,可以提供新的视角,为肾脏疾病的发病机制和治疗。
关键词: Fractalkine,CX3CL1,趋化因子受体,CX3CR1,肾脏疾病,肾移植。
Current Gene Therapy
Title:CX3CL1/CX3CR1 Axis, as the Therapeutic Potential in Renal Diseases: Friend or Foe?
Volume: 17 Issue: 6
关键词: Fractalkine,CX3CL1,趋化因子受体,CX3CR1,肾脏疾病,肾移植。
摘要: The fractalkine receptor chemokine (C-X3-C motif) receptor 1 (CX3CR1) and its highly selective ligand CX3CL1 mediate chemotaxis and adhesion of immune cells, which are involved in the pathogenesis and progression of numerous inflammatory disorders and malignancies. The CX3CL1/CX3CR1 axis has recently drawn attention as a potential therapeutic target because it is involved in the ontogeny, homeostatic migration, or colonization of renal phagocytes. We performed a Medline/PubMed search to detect recently published studies that explored the relationship between the CX3CL1/CX3CR1 axis and renal diseases and disorders, including diabetic nephropathy, renal allograft rejection, infectious renal diseases, IgA nephropathy, fibrotic kidney disease, lupus nephritis and glomerulonephritis, acute kidney injury and renal carcinoma. Most studies demonstrated its role in promoting renal pathopoiesis; however, several recent studies showed that the CX3CL1/CX3CR1 axis could also reduce renal pathopoiesis. Thus, the CX3CL1/CX3CR1 axis is now considered to be a double-edged sword that could provide novel perspectives into the pathogenesis and treatment of renal diseases and disorders.
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CX3CL1/CX3CR1 Axis, as the Therapeutic Potential in Renal Diseases: Friend or Foe?, Current Gene Therapy 2017; 17 (6) . https://dx.doi.org/10.2174/1566523218666180214092536
DOI https://dx.doi.org/10.2174/1566523218666180214092536 |
Print ISSN 1566-5232 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5631 |
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