RESEARCH A new mechanism of actio e n

Full list of author information is available at the end of the articleBackground Diabetic nephropathy (DN) and several other chronic kidney diseases are characterized by tubular and intersti-tial fibrosis, which are primarily responsible for acceler-ating the progression to end-stage renal disease (ESRD) [1-3]. The epithelial-mesenchymal transition (EMT) of tubular epithelial cells is a process that sustains these events [4,5], and it is triggered by many factors [6-9]. A recent work of ours highlighted the central role of FGF-2 in EMT. Heparanase-1 (HPSE) is needed for EMT and by regulating syndecan-1 (SDC1) and MMP9 it sustains the FGF-2 autocrine loop [10]. HPSE is an endo-β-D-glucuronidase that cleaves heparan sulfate (HS). It takes part in extracellular matrix (ECM) remodeling and deg-radation, regulating the release of many HS-bonded molecules, such as growth factors, chemokines, cyto-kines, and enzymes, that are involved in inflammation, wound healing and tumor invasion [11,12]. A body o