Huang C is funded by Australian National Health and Medical Research Council (NHMRC) Peter Doherty Early Career Fellowship (APP1110560). ![]() This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: All relevant data are within the paper.įunding: This work was supported by Juvenile Diabetes Research Foundation International (-258-Q-R). ![]() Received: DecemAccepted: JanuPublished: February 9, 2018Ĭopyright: © 2018 Huang et al. PLoS ONE 13(2):Įditor: Michael Bader, Max Delbruck Centrum fur Molekulare Medizin Berlin Buch, GERMANY (2018) The KCa3.1 blocker TRAM34 reverses renal damage in a mouse model of established diabetic nephropathy. These results indicate that KCa3.1 blockade effectively reverses established diabetic nephropathy in this rodent model and provides a basis for progressing to human studies.Ĭitation: Huang C, Zhang L, Shi Y, Yi H, Zhao Y, Chen J, et al. The results clearly demonstrate that TRAM34 reduced albuminuria, decreased inflammatory markers and reversed extracellular matrix deposition in kidneys via inhibition of the TGF-β1 signaling pathway. Albuminuria was assessed, inflammatory markers (CD68, F4/80) and extracellular matrix deposition (type I collagen and fibronectin) in the kidneys were examined. At 24 weeks, at which time we have previously demonstrated albuminuria and pathological changes of diabetic nephropathy, mice were randomised to receive TRAM34 subcutaneously, a highly selective inhibitor of potassium channel KCa3.1 or DMSO (vehicle) for a further 14 weeks. In this studies, eNOS-/- mice were administered with streptozotocin to induce diabetes. The clinical scenario is that patients with diabetes mellitus often present with established kidney damage and need effective treatments to repair and reverse the kidney damage. However, targeting these pathways once kidney disease is established, remain unsatisfactory. Strategies to target various signaling pathways to prevent DN have been intensively investigated in animal models and many have been proved to be promising. ![]() Despite optimal control of hyperglycaemia, hypertension, and dyslipidaemia, the number of patients with diabetic nephropathy (DN) continues to grow.
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