Role of Receptor Tyrosine Kinase Signaling in Renal Fibrosis

• Main Authors: Feng Liu, Shougang Zhuang
• Format: Article
• Language: English
• Published: MDPI AG 2016-06-01
• Series: International Journal of Molecular Sciences
• Subjects: receptor tyrosine kinases; platelet-derived growth factors receptor; fibroblast growth factor receptor; vascular endothelial growth factors receptor; epidermal growth factor receptor; insulin-like growth factor receptor; discoidin domain receptors; growth arrest-specific gene; tyrosine kinase inhibitors; renal fibrosis
• Online Access: http://www.mdpi.com/1422-0067/17/6/972

Renal fibrosis can be induced in different renal diseases, but ultimately progresses to end stage renal disease. Although the pathophysiologic process of renal fibrosis have not been fully elucidated, it is characterized by glomerulosclerosis and/or tubular interstitial fibrosis, and is believed to be caused by the proliferation of renal inherent cells, including glomerular epithelial cells, mesangial cells, and endothelial cells, along with defective kidney repair, renal interstitial fibroblasts activation, and extracellular matrix deposition. Receptor tyrosine kinases (RTKs) regulate a variety of cell physiological processes, including metabolism, growth, differentiation, and survival. Many studies from in vitro and animal models have provided evidence that RTKs play important roles in the pathogenic process of renal fibrosis. It is also showed that tyrosine kinases inhibitors (TKIs) have anti-fibrotic effects in basic research and clinical trials. In this review, we summarize the evidence for involvement of specific RTKs in renal fibrosis process and the employment of TKIs as a therapeutic approach for renal fibrosis.