Microbiota-derived corisin accelerates kidney fibrosis by promoting cellular aging
Taro Yasuma1,2,3, Hajime Fujimoto4, Corina N D'Alessandro-Gabazza1,2,5
1Department of Immunology, Mie University Faculty and Graduate School of Medicine, Edobashi 2-174, Tsu, Mie, Japan.
Nature Communications
|August 25, 2025
Summary
Diabetic kidney disease is worsened by corisin, a peptide from gut microbes. Targeting corisin with antibodies may offer a new therapy for diabetic nephropathy.
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.
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