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Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging.

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Area of Science:

  • Nephrology
  • Microbiology
  • Immunology

Background:

  • Diabetic nephropathy is a leading cause of chronic kidney disease (CKD) with limited anti-fibrotic treatments.
  • Gut microbiota-derived metabolites are increasingly implicated in metabolic diseases.

Purpose of the Study:

  • To identify novel drivers of diabetic kidney fibrosis.
  • To investigate the role of microbiota-derived peptides in diabetic nephropathy progression.

Main Methods:

  • Serum corisin levels were measured in patients with diabetic CKD and healthy controls.
  • Corisin's role in kidney fibrosis was assessed in a murine model.
  • Monoclonal anti-corisin antibodies were used for therapeutic intervention in mice.
  • Molecular dynamics simulations and cellular assays were employed to elucidate corisin's mechanism of action.

Main Results:

  • Corisin levels were significantly elevated in diabetic CKD patients and correlated with disease severity and renal function decline.
  • Elevated corisin exacerbated kidney fibrosis, inflammation, and renal impairment in mice.
  • Anti-corisin antibody treatment ameliorated nephropathy in diabetic mice.
  • Corisin was shown to interact with human serum albumin and accelerate cellular senescence, epithelial-mesenchymal transition, and apoptosis in kidney cells.

Conclusions:

  • Corisin is a critical mediator of diabetic kidney fibrosis progression.
  • Targeting corisin represents a potential therapeutic strategy for diabetic nephropathy.