The loss of Kruppel-like factor 15 in Foxd1⁺ stromal cells exacerbates kidney fibrosis.

ABSTRACT: Large epidemiological studies clearly demonstrate that multiple episodes of acute kidney injury contribute to the development and progression of kidney fibrosis. Although our understanding of kidney fibrosis has improved in the past two decades, we have limited therapeutic strategies to halt its progression. Myofibroblast differentiation and proliferation remain critical to the progression of kidney fibrosis. Although canonical Wnt signaling can trigger the activation of myofibroblasts in the kidney, mediators of Wnt inhibition in the resident progenitor cells are unclear. Recent studies demonstrate that the loss of a Krüppel-like factor 15 (KLF15), a kidney-enriched zinc-finger transcription factor, exacerbates kidney fibrosis in murine models. Here, we tested whether Klf15 mRNA and prote

SUBMITTER: Gu X 

PROVIDER: S-EPMC5651204 | biostudies-literature | 2017 Nov

REPOSITORIES: biostudies-literature