Abstract
Chronic kidney disease (CKD) caused by renal fibrosis is an important public health concern. It is therefore necessary to understand the molecular pathogenesis of renal fibrosis in order to develop novel therapeutic strategies. KLF4 is the most extensively studied factor among the various members of the Krüppel-like factor (KLF) family of zinc finger-containing transcription factors. Many studies have demonstrated that KLF4 inhibits the activation of myofibroblasts and exerts an inhibitory effect on fibrosis. However, other studies have indicated that KLF4 may promote renal fibrosis. These controversial results suggest that KLF4 may be crucially involved in the development of renal fibrosis, although the underlying mechanism(s) remain unclear. Here, we summarize the recent progress made in understanding the role of KLF4 in renal fibrosis. Together, these findings suggest that KLF4 may participate in the development of renal fibrosis, but that its inhibition of fibrosis is greater than its promotion of the condition, which suggests that KLF4 may serve as a novel therapeutic target for renal fibrosis.
Highlights
Renal fibrosis is characterized by excessive proliferation of fibroblasts and increased deposition of extracellular matrix (ECM), which together lead to extensive scarring, renal artery stenosis and chronic inflammatory cell infiltration (Li et al, 2015)
KLF4 can induce the transformation of primary fibroblasts (Rowland et al, 2005) but can induce fibroblasts to become pluripotent stem cells in mice (Takahashi and Yamanaka, 2006; Okita et al, 2007; Wernig et al, 2007)
These findings make the function of KLF4 in renal fibrosis confusing; the findings described above indicate that KLF4 participates in the development of renal fibrosis and that its inhibition of fibrosis is greater than its promotion of the condition
Summary
Renal fibrosis is characterized by excessive proliferation of fibroblasts and increased deposition of extracellular matrix (ECM), which together lead to extensive scarring (fibrotic tubular and glomerular sclerosis), renal artery stenosis and chronic inflammatory cell infiltration (Li et al, 2015). In an animal model of diabetic nephropathy, KLF4 expression was significantly decreased in renal tubular cells (Mreich et al, 2015). KLF4 is involved in renal fibrosis by regulating inflammation (Mreich et al, 2015).
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