Abstract

Abstract renal fibrosis is a process of excess accumulation and deposition of extracellular matrix (ECM) proteins in kidney. Transforming growth factor-beta (TGF-β) plays a vital role in accumulation of ECM through initiating phosphorylated Smad2/3. Whether activin receptor-like kinase 7 (ALK7), a member of TGF-β superfamily, was involved in renal interstitial fibrosis remains unclear. The aim of this study was to investigate whether ALK7 participates in renal fibrosis via regulating phosphorylated Smad2/3 in high-fat diet (HFD) rats. Forty male Sprague-Dawley (SD) rats were randomly assigned to 4 groups: control, HFD, HFD + Vehicle and HFD + ALK7-siRNA. The metabolic index, ALK7 expression and collagen deposition in renal tissue were measured, and renal fibrosis was evaluated by stained with hematoxylin and eosin, Masson's trichrome and periodic acid-Schiff. HFD induced insulin resistant state accompanied by increased blood glucose, cholesterol and triglyceride levels in rats. HFD enhanced the expression of ALK7 which involved the renal fibrosis, which was accompanied by increased phosphorylated Smad2/3. Additionally, ALK7 gene silencing reduced renal fibrosis along with decreased Smad2/3 phosphorylation. ALK7 gene silencing plays a protective role in renal fibrosis in rats with HFD and might be an effective treatment target of HFD-induced renal fibrosis.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call