Continuous AMD3100 Treatment Worsens Renal Fibrosis through Regulation of Bone Marrow Derived Pro-Angiogenic Cells Homing and T-Cell-Related Inflammation.

Continuous AMD3100 Treatment Worsens Renal Fibrosis through Regulation of Bone Marrow Derived Pro-Angiogenic Cells Homing and T-Cell-Related Inflammation.

AMD3100 is a small molecule inhibitor of chemokine receptor type 4 (CXCR4), which is located in the cell membranes of CD34+ cells and a variety of inflammatory cells and has been reported to reduce organ fibrosis in the lung, liver and myocardium. However, the effect of AMD3100 on renal fibrosis is...

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Bibliographic Details
Main Authors: Juan Yang, Fengming Zhu, Xiaohui Wang, Weiqi Yao, Meng Wang, Guangchang Pei, Zhizhi Hu, Yujiao Guo, Zhi Zhao, Pengge Wang, Jingyi Mou, Jie Sun, Rui Zeng, Gang Xu, Wenhui Liao, Ying Yao
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2016-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC4763993?pdf=render

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http://europepmc.org/articles/PMC4763993?pdf=render

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