Bowers Stephanie L K, Davis-Rodriguez Stephanie, Thomas Zachary M, Rudomanova Valeria, Bacon W Clark, Beiersdorfer Alex, Ma Qing, Devarajan Prasad, Blaxall Burns C
Department of Pediatrics, University of Cincinnati College of Medicine , Cincinnati, Ohio.
The Heart Institute, Cincinnati Children's Hospital Medical Center , Cincinnati, Ohio.
Am J Physiol Renal Physiol. 2019 Jun 1;316(6):F1293-F1298. doi: 10.1152/ajprenal.00117.2019. Epub 2019 Apr 24.
Fibrosis is a common feature of chronic kidney disease; however, no clinical therapies effectively target the progression of fibrosis. Inhibition of fibronectin polymerization with the small peptide pUR4 attenuates fibrosis in the liver and heart. Here, we show that pUR4 decreases renal fibrosis and tissue remodeling using a clinically relevant model of kidney injury, unilateral ischemia-reperfusion. This work highlights the benefits of inhibiting matrix polymerization, alone or in conjunction with cell-based therapies, as a novel approach to diminish the maladaptive responses to ischemic kidney injury that lead to chronic renal failure.
纤维化是慢性肾脏病的常见特征;然而,尚无临床疗法能有效靶向纤维化的进展。用小肽pUR4抑制纤连蛋白聚合可减轻肝脏和心脏的纤维化。在此,我们使用与临床相关的肾损伤模型——单侧缺血再灌注,证明pUR4可减少肾纤维化和组织重塑。这项工作突出了单独或与基于细胞的疗法联合抑制基质聚合的益处,这是一种减少导致慢性肾衰竭的对缺血性肾损伤的适应性不良反应的新方法。