Related Experiment Video

Updated: Jun 12, 2025

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
10:37

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

101

CXCL5 inhibition improves kidney function by protecting renal tubular epithelial cells in diabetic kidney disease

Ching Chen1, Liang-Yu Lin2, Yen-Wen Wu3

  • 1Department and Institute of Pharmacology, National Yang Ming Chiao Tung University, Taipei, Taiwan; School of Medicine, National Yang Ming Chiao Tung University, Taipei, Taiwan.

Clinical Immunology (Orlando, Fla.)
|September 26, 2024
PubMed

Insights

Targeting CXCL5, a key inflammatory factor, shows promise for treating diabetic kidney disease (DKD). Inhibiting CXCL5 improved kidney function and reduced damage in preclinical models, suggesting new therapeutic strategies for DKD.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Diabetic kidney disease (DKD) is a major complication of diabetes, exacerbated by inflammation.
  • Elevated levels of CXCL5 are observed in both clinical and experimental diabetes, suggesting its role in DKD pathogenesis.

Purpose of the Study:

  • To investigate the impact and underlying mechanisms of CXCL5 in the development and progression of diabetic kidney disease.
  • To evaluate the therapeutic potential of inhibiting CXCL5 in DKD.

Main Methods:

  • DKD patients and control subjects were enrolled, with urine albumin-to-creatinine ratio used for stratification.
  • Leprdb/db mice and CXCL5-knockout diabetic mice served as DKD models.
  • In vitro studies utilized human renal tubular epithelial cells stimulated with high glucose.

Main Results:

  • Circulating CXCL5 levels were significantly higher in DKD patients compared to non-DKD subjects.
  • CXCL5 inhibition (via antibodies or genetic knockout) improved kidney function, reduced tubular injury, and ameliorated renal fibrosis in mouse models.
  • In vitro, CXCL5 inhibition decreased inflammatory, fibrotic, and apoptotic markers by suppressing JNK/c-JUN/p65 signaling pathways.

Conclusions:

  • CXCL5 plays a significant role in the pathogenesis of diabetic kidney disease.
  • Inhibiting CXCL5 demonstrates therapeutic potential for treating DKD by mitigating inflammation, fibrosis, and apoptosis.
  • Anti-CXCL5 strategies represent a promising avenue for future DKD treatments.
Keywords:
Chemokine CXC motif ligand 5Diabetic kidney diseaseFibrosisInflammationRenal tubular epithelial cell

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