Renal tubular injury exacerbated by Vasohibin-1 deficiency in a murine cisplatin-induced acute kidney injury model.

Renal tubular injury exacerbated by Vasohibin-1 deficiency in a murine cisplatin-induced acute kidney injury model. Am J Physiol Renal Physiol. 2019 May 15;: Authors: Tanimura S, Tanabe K, Miyake H, Masuda K, Tsushida K, Morioka T, Sugiyama H, Sato Y, Wada J Abstract Acute kidney injury (AKI) is frequently encountered in clinical practice, particularly secondary to cardiovascular surgery and administration of nephrotoxic agents, and is increasingly recognized for initiating a transition to chronic kidney disease. Clarifying the pathogenesis of AKI could facilitate the development of novel preventive strategies because the occurrence of hospital-acquired AKI is often anticipated. Vasohibin-1 (VASH1) was initially identified as an antiangiogenic factor derived from endothelial cells. VASH1 expression in endothelial cells has subsequently been reported to enhance cellular stress tolerance. Considering the importance of maintaining peritubular capillaries in preventing the progression of AKI, this study aimed to examine whether VASH1 deletion is involved in the pathogenesis of cisplatin-induced AKI. For this, we injected male C57BL/6J wild-type (WT) and VASH1 heterozygous knockout (VASH1+/-) mice with either 20 mg/kg of cisplatin or a vehicle solution intraperitoneally. Seventy-two hours after cisplatin injection, increased serum creatinine concentrations and renal tubular injury accompanied by apoptosis and oxidative stress were more pr...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research