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Unlocking the therapeutic potential of the NFAT pathway in kidney diseases

Shruti Shreya1, Neha Dagar1, Anil Bhanudas Gaikwad2

  • 1Department of Pharmacy, Birla Institute of Technology and Science, Pilani Campus, Pilani, Rajasthan, 333031, India.

Naunyn-Schmiedeberg'S Archives of Pharmacology
|March 15, 2025
PubMed

Insights

Nuclear factor of activated T cells (NFAT) plays a key role in kidney disease by promoting cell death and fibrosis. Downregulating NFAT shows promise as a therapeutic strategy for mitigating kidney damage.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • The nuclear factor of activated T cells (NFAT) is a transcription factor crucial in cellular processes.
  • NFAT is implicated in the pathogenesis of kidney diseases, contributing to renal tubular epithelial cell apoptosis.
  • Elevated NFAT levels correlate with kidney disease progression.

Purpose of the Study:

  • To review the role and regulation of NFAT in kidney disease pathogenesis.
  • To highlight preclinical evidence supporting NFAT downregulation as a therapeutic strategy.
  • To establish a foundation for future clinical investigations into NFAT-targeted therapies.

Main Methods:

  • Review of preclinical studies on NFAT in kidney disease.
  • Analysis of the NFAT/calcineurin signaling pathway in renal pathophysiology.
  • Examination of potential therapeutic agents targeting NFAT.

Main Results:

  • NFAT activation, regulated by calcium and calcineurin, leads to nuclear localization and promotes kidney cell apoptosis, inflammation, and fibrosis.
  • Downregulation or silencing of NFAT has been shown to mitigate kidney disease in preclinical models.
  • Several agents like anandamide, 11R-VIVIT, and maxacalcitol are being investigated for their potential to regulate NFAT.

Conclusions:

  • NFAT is a significant contributor to kidney disease pathogenesis.
  • Targeting NFAT represents a promising therapeutic avenue for kidney disease.
  • Further clinical research is warranted to translate these preclinical findings into effective treatments.
Keywords:
CalcineurinCalciumKidney diseaseNFAT signallingTherapeutic targets

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