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  • Year in Review
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Renal fibrosis in 2015

Understanding the mechanisms of kidney fibrosis

The year 2015 has seen great progress in the renal fibrosis field, as key studies began to build a consensus on the importance of epithelial-to-mesenchymal transition, cell cycle arrest, and defective metabolism in the pathogenesis of kidney fibrosis. New findings also point to a role of developmental signalling in renal fibrogenesis.

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Figure 1: Studies have highlighted important roles for varying tubular responses such as partial epithelial-to-mesenchymal transition (EMT), cell cycle arrest and defective metabolism in driving renal fibrosis.

References

  1. Humphreys, B. D. et al. Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. Am. J. Pathol. 176, 85–97 (2010).

    Article  CAS  Google Scholar 

  2. Grande, M. T. et al. Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease. Nat. Med. 21, 989–997 (2015).

    Article  CAS  Google Scholar 

  3. Lovisa, S. et al. Epithelial-to-mesenchymal transition induces cell cycle arrest and parenchymal damage in renal fibrosis. Nat. Med. 21, 998–1009 (2015).

    Article  CAS  Google Scholar 

  4. Kang, H. M. et al. Defective fatty acid oxidation in renal tubular epithelial cells has a key role in kidney fibrosis development. Nat. Med. 21, 37–46 (2015).

    Article  CAS  Google Scholar 

  5. Gomez, I. G. et al. Anti-microRNA-21 oligonucleotides prevent Alport nephropathy progression by stimulating metabolic pathways. J. Clin. Invest. 125, 141–156 (2015).

    Article  Google Scholar 

  6. Zhou, D. et al. Sonic hedgehog is a novel tubule-derived growth factor for interstitial fibroblasts after kidney injury. J. Am. Soc. Nephrol. 25, 2187–2200 (2014).

    Article  CAS  Google Scholar 

  7. Kramann, R. et al. Perivascular Gli1+ progenitors are key contributors to injury-induced organ fibrosis. Cell Stem Cell 16, 51–66 (2015).

    Article  CAS  Google Scholar 

  8. Kramann, R. et al. Pharmacological GLI2 inhibition prevents myofibroblast cell-cycle progression and reduces kidney fibrosis. J. Clin. Invest. 125, 2935–2951 (2015).

    Article  Google Scholar 

  9. Xiao, L. et al. Sustained activation of Wnt/β-catenin signaling drives AKI to CKD progression. J. Am. Soc. Nephrol. 27, http://dx.doi.org/10.1681/ASN.2015040449 (2015).

  10. Zhou, L. et al. Multiple genes of the renin−angiotensin system are novel targets of Wnt/β-catenin signaling. J. Am. Soc. Nephrol. 26, 107–120 (2015).

    Article  CAS  Google Scholar 

Download references

Acknowledgements

The author's work is supported by NIH grants DK064005, DK091239 and DK106049, and National Science of Foundation of China grants 81130011 and 81521003.

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Correspondence to Youhua Liu.

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Zhou, D., Liu, Y. Understanding the mechanisms of kidney fibrosis. Nat Rev Nephrol 12, 68–70 (2016). https://doi.org/10.1038/nrneph.2015.215

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