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Extracellular vesicle miR-93-5p cargo regulates glomerular endothelial cell damage in Alport syndrome

Charmi Dedhia1, Valentina Villani1, Xiaogang Hou1

  • 1The GOFARR Laboratory, The Saban Research Institute, Division of Urology, and.

JCI Insight
|March 23, 2026
PubMed

Insights

MicroRNA-93-5p (miR-93-5p) is crucial for mitigating glomerular damage in Alport syndrome. Extracellular vesicles from human amniotic fluid stem cells (hAFSC-EVs) deliver miR-93-5p, restoring kidney function by regulating endothelial cell pathways.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Glomerular cell microRNA (miRNA) expression changes are linked to kidney disease.
  • Alport syndrome, a genetic kidney disorder, involves progressive glomerular damage.

Purpose of the Study:

  • To investigate the role of miR-93-5p in Alport syndrome-related glomerular damage.
  • To determine if extracellular vesicles from human amniotic fluid stem cells (hAFSC-EVs) exert therapeutic effects via their miR-93-5p content.

Main Methods:

  • Spatial transcriptomics and molecular imaging were used to analyze kidney tissues and patient biopsies.
  • miR-93-5p was silenced in hAFSC-EVs to assess its impact on cellular function and disease models.
  • In vitro and in vivo assays evaluated glomerular endothelial cell function and kidney function restoration.

Main Results:

  • miR-93-5p was downregulated in glomerular endothelial cells during Alport syndrome progression.
  • hAFSC-EVs delivered miR-93-5p to regulate VEGFR1 and VEGFR2 signaling, restoring endothelial cell biology.
  • Silencing miR-93-5p in hAFSC-EVs abrogated their therapeutic effects in vitro and in vivo.
  • hAFSC-EVs reversed disease-associated pathways and stimulated proregenerative processes in the glomerulus.

Conclusions:

  • miR-93-5p plays a critical role in glomerular endothelial cell function in Alport syndrome.
  • hAFSC-EVs mediate therapeutic benefits through miR-93-5p cargo transfer, highlighting a novel treatment strategy for Alport syndrome.
Keywords:
Cell biologyChronic kidney diseaseNephrology

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