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Related Experiment Video

Updated: Jun 5, 2026

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium
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Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.

Jing Liu1, Mingzhuo Zhang1, Yan Ge1

  • 1Division of Nephrology, Department of Medicine, University of Toledo College of Medicine, Toledo, OH, USA.

Molecular Therapy : the Journal of the American Society of Gene Therapy
|July 31, 2025
PubMed
Summary

Melanocortin therapy, particularly targeting melanocortin 5 receptor (MC5R) in podocytes, shows promise for treating membranous nephropathy by inhibiting complement activation.

Keywords:
ACTHPPARγautoimmunecomplement amplification loopglomerular diseasemembranous nephropathynephrotic syndrome

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Area of Science:

  • Nephrology
  • Immunology
  • Pharmacology

Background:

  • Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults.
  • Current treatments for MN have limitations, and underlying mechanisms require further elucidation.
  • Melanocortin therapy shows potential for MN, but its precise role and targets are unclear.

Purpose of the Study:

  • To investigate the therapeutic potential and mechanisms of melanocortin agents in a mouse model of THSD7A-associated membranous nephropathy.
  • To determine the role of melanocortin 5 receptor (MC5R) in podocytes in the context of MN pathogenesis and treatment.

Main Methods:

  • Utilized a heterologous mouse model of THSD7A-associated membranous nephropathy.
  • Administered various melanocortin agents, including repository corticotropin injection, NDP-MSH, and PG-901.
  • Generated MC5R knockout mice and performed podocyte-specific MC5R reconstitution experiments.
  • Analyzed glomerular deposition of complement components (C3, C5b-9) and expression of complement factors B and D.
  • Investigated the involvement of peroxisome proliferator-activated receptor gamma (PPARγ) signaling.

Main Results:

  • Melanocortin agents attenuated proteinuria and ameliorated glomerulopathy in the MN mouse model.
  • MC5R knockout exacerbated MN and abolished the therapeutic effects of melanocortins.
  • Podocyte MC5R was essential for melanocortin-mediated protection against MN.
  • MC5R agonism reduced glomerular C5b-9 and C3 deposition by inhibiting podocyte expression of complement factors B and D via a PPARγ-dependent mechanism.

Conclusions:

  • Podocyte MC5R plays a critical protective role in membranous nephropathy.
  • Melanocortin therapy, through MC5R, offers a novel therapeutic strategy for MN by modulating the complement cascade.
  • Targeting MC5R in podocytes may represent a new avenue for treating membranous nephropathy.