Table 1 Key facts of renal fibrosis pathogenesis

A variety of cells contribute to interstitial fibrosis, including fibroblasts, dendritic cells, lymphocytes, and monocyte/macrophages

Tubular epithelial cells possibly contribute to fibrosis as they are damaged and undergo a putative epithelial-mesenchymal transition (EMT)/phenotype (EMP). Endothelial cells also possibly contribute to fibrosis through an endothelial to mesenchymal transition (EndoMT). However, despite evidence for these processes, some question EMT and EndoMT

Cellular damage is thought to contribute to the release of molecular mediators, many of which are pro-fibrotic, including tumor growth factor beta (TGF-β), a major fibrogenic and inflammatory cytokine. Other growth factors include bone morphogenic protein (BMP), platelet-derived growth factor (PDGF), and hepatocyte growth factor (HGF)

Fibrosis ultimately occurs through the deposition of extracellular matrix (ECM), including collagen, proteoglycans, and admixed ECM molecules such as fibronectin, biglycan, decorin, tissue transglutaminase (tTG), matrix metalloproteinase (MMP), tissue plasminogen activator (tPA), and laminin