CXCR6 is a critical mechanistic mediator of Angiotensin II-induced renal injury and fibrosis via immune cell and fibroblast regulation.
Should not change clinical practice in hypertensive nephropathy; hypothesis-generating for CXCR6-targeted therapies in renal fibrosis.
Our results indicate that CXCR6 plays a pivotal role in the development of Ang II-induced renal injury and fibrosis through regulation of macrophage and T-cell infiltration and bone marrow-derived fibroblast accumulation.
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Xia et al. (2014) studied this question.