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Podocyte dysfunction driven by heme in sickle-cell nephropathy.

Chloé Ben Ali1, Antoine Morel1,2, Marion Morvan1

  • 1Institut National de la Santé Et de la Recherche Médicale (INSERM), Institut Mondor de Recherche Biomédicale (INSERM U955), Université Paris Est Créteil, 94010, Créteil, France.

Scientific Reports
|July 27, 2025
PubMed
Summary
This summary is machine-generated.

Heme damages kidney podocytes in sickle-cell nephropathy through oxidative stress and other pathways. This finding offers new insights for treating sickle-cell disease complications.

Keywords:
Cellular stressHemeHemolysisOxidative stressPodocyte

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Area of Science:

  • Nephrology
  • Hematology
  • Molecular Biology

Background:

  • Sickle-cell disease (SCD) causes kidney damage (sickle-cell nephropathy, SCN) linked to hemolysis and heme release.
  • The precise molecular mechanisms of heme-induced podocyte injury in SCN are not fully understood.

Purpose of the Study:

  • To investigate the effects of heme on human podocyte function.
  • To explore the role of oxidative stress and related pathways in heme-induced podocyte damage.
  • To correlate in vitro findings with renal biopsy data from FSGS and SCD-FSGS patients.

Main Methods:

  • Human podocytes were exposed to hemin (5 μM) for 4 and 24 hours, with and without N-acetyl cysteine (NAC).
  • Assessed podocyte cytoskeleton, apoptosis, oxidative stress markers, DNA damage, mitochondrial/ER function, and NF-κB activation.
  • Analyzed renal biopsy specimens from controls, FSGS, and SCD-FSGS patients for HO-1, BiP, and synaptopodin expression.

Main Results:

  • Hemin exposure caused podocyte cytoskeleton damage and apoptosis within 4 hours.
  • At 24 hours, hemin increased heme oxygenase-1 (HO-1) expression, oxidative stress, DNA damage, and organelle dysfunction.
  • NAC partially mitigated hemin-induced damage, highlighting oxidative stress's role but indicating other mechanisms are involved.
  • Renal biopsies showed elevated HO-1 and BiP, with reduced synaptopodin in podocytes of FSGS and SCD-FSGS patients.

Conclusions:

  • Heme directly damages kidney podocytes via oxidative stress and other molecular pathways in SCN.
  • Elevated HO-1 and BiP in patient biopsies confirm in vitro findings and suggest podocyte injury in FSGS and SCD.
  • This research provides a deeper understanding of SCN pathogenesis and potential therapeutic targets.