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Snail and kidney fibrosis.

Noémie Simon-Tillaux1, Alexandre Hertig1,2

  • 1French National Institute of Health and Medical Research (INSERM), UMR_S1155, Remodeling and Repair of Renal Tissue, Hôpital Tenon, Paris, France.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
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PubMed
Summary

Snail family zinc finger 1 (SNAI1) drives kidney fibrosis by controlling cell reprogramming and metabolism during acute kidney injury (AKI). Targeting SNAI1 shows promise in preventing kidney scarring in animal models.

Keywords:
acute kidney injuryepitheliumfibroblastsfibrosisSNAIL

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Developmental Biology

Background:

  • Snail family zinc finger 1 (SNAI1) is a transcription factor crucial for renal development.
  • SNAI1 is re-expressed in acute kidney injury (AKI), a condition leading to kidney fibrosis.
  • Its regulation is complex and impacts key fibrotic processes.

Purpose of the Study:

  • To review the role of SNAI1 in renal fibrogenesis.
  • To detail SNAI1 interactions with AKI-associated signaling pathways.
  • To discuss therapeutic targeting of SNAI1 in AKI models.

Main Methods:

  • Literature review focusing on SNAI1's molecular functions in kidney injury.
  • Analysis of signaling pathways influenced by SNAI1.
  • Examination of preclinical studies targeting SNAI1 for fibrotic disease.

Main Results:

  • SNAI1 orchestrates tubular epithelial cell reprogramming, fatty acid metabolism shutdown, cell cycle arrest, and inflammation.
  • SNAI1 interacts with multiple signaling pathways implicated in AKI.
  • Targeting SNAI1 has shown potential in mitigating renal fibrogenesis in animal models.

Conclusions:

  • SNAI1 is a central regulator of renal fibrogenesis in AKI.
  • Understanding SNAI1's interactions is key to developing antifibrotic therapies.
  • Targeting SNAI1 represents a promising therapeutic strategy for preventing kidney scarring.