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Related Experiment Video

Updated: May 15, 2025

Use of Ultra-high Field MRI in Small Rodent Models of Polycystic Kidney Disease for In Vivo Phenotyping and Drug Monitoring
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Targeting Dysregulated Epigenetic Modifiers With Kidney-Targeted Nanotherapeutics for Polycystic Kidney Disease.

Joshua Giblin1, Rowan Simon1, Jose Zarate-Diaz1

  • 1Alfred E. Mann Department of Biomedical Engineering, University of Southern California, Los Angeles, California, USA.

Journal of Biomedical Materials Research. Part A
|April 9, 2025
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Summary

New research identifies epigenetic targets Brd4 and BMi1 for Autosomal dominant polycystic kidney disease (ADPKD). Inhibiting these targets with drugs, delivered via kidney-targeting micelles, significantly reduced ADPKD cell proliferation, offering a novel therapeutic strategy.

Keywords:
ADPKDchronic kidney diseasedrug deliveryepigeneticsnanomedicine

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Area of Science:

  • Nephrology
  • Genetics
  • Epigenetics

Background:

  • Autosomal dominant polycystic kidney disease (ADPKD) is a prevalent genetic kidney disorder.
  • Current treatments like tolvaptan have limitations, including side effects and poor adherence.
  • Epigenetic alterations are implicated in ADPKD, but specific modulators remain underexplored therapeutic targets.

Purpose of the Study:

  • To investigate the role of epigenetic modulators in ADPKD.
  • To evaluate the therapeutic potential of inhibiting upregulated epigenetic factors Brd4 and BMi1 in ADPKD.
  • To assess the efficacy of kidney-targeting micelles (KM) for delivering epigenetic drugs to renal cells.

Main Methods:

  • Analysis of gene expression of epigenetic modulators in ADPKD patient-derived cyst cells.
  • Inhibition of Brd4 and BMi1 using small molecule drugs (AZD-5153 and PTC-209).
  • In vitro assessment of drug efficacy in ADPKD cells, 3D cyst models, and murine Pkd1 null cells, including drug delivery via KMs.

Main Results:

  • Brd4 and BMi1 were found to be upregulated in ADPKD patient cells.
  • Inhibition of Brd4 and BMi1 with AZD-5153 and PTC-209 significantly slowed ADPKD cell proliferation.
  • Combined drug treatment within KMs demonstrated a synergistic effect in reducing proliferation in ADPKD models.

Conclusions:

  • Brd4 and BMi1 represent novel therapeutic targets for ADPKD.
  • Targeting the epigenome with kidney-targeted nanomedicine offers a promising new strategy for ADPKD treatment.
  • This approach shows potential for improved drug delivery and synergistic therapeutic effects in ADPKD.