ACKR3 and Increased circulating aldosterone concentration: Utilising DOCA-UNX-induced mineralocorticoid excess induced hypertension and fibrosis in C57BL/6 mice, we have shown that CXCR7 antagonist monoclonal antibody treatment significantly attenuated cardiac and renal fibrosis, and related fibrotic gene expression without affecting blood pressure, cardiac chamber sizes and function.