Related Experiment Video

Updated: Sep 25, 2025

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
10:31

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

Published on: May 2, 2025

313

Activation of Complement Pathways in Kidney Tissue May Mediate Tubulointerstitial Injury in Diabetic Nephropathy

Shimin Jiang1, Yuanyuan Jiao2, Guming Zou1

  • 1Department of Nephrology, China-Japan Friendship Hospital, Beijing, China.

Frontiers in Medicine
|April 28, 2022
PubMed
Abstract

Insights

Complement activation, specifically involving C3 and C1q deposits, is linked to tubulointerstitial injury and kidney function decline in diabetic nephropathy (DN). This suggests complement pathways are key drivers of DN progression.

Area of Science:

  • Nephrology
  • Immunology
  • Genetics

Background:

  • Diabetic nephropathy (DN) involves tubulointerstitial injury, a key factor in disease progression.
  • Complement-related genes may play a role in the mechanisms underlying tubulointerstitial injury in DN.

Purpose of the Study:

  • To investigate the association between complement-related genes and tubulointerstitial injury in DN.
  • To explore the link between complement pathway activation and DN progression.

Main Methods:

  • Weighted gene co-expression network analysis (WGCNA) of microarray data from DN patients and controls.
  • Analysis of C3 and C1q deposits in kidney tissues and their association with renal outcomes.
  • Immunohistochemical analysis of complement factors (C3, C1q, C5b-9, MBL, factor B) in renal tubulointerstitium.

Main Results:

  • A gene co-expression network identified a 'black module' positively correlated with tubulointerstitial injury.
  • C3 was significantly overexpressed in DN tubulointerstitial tissue and negatively correlated with estimated glomerular filtration rate (eGFR).
  • Codeposits of C3 and C1q were independently associated with adverse renal outcomes in DN patients; higher expression of C1q, C3, C5b-9, MBL, or factor B correlated with kidney failure.

Conclusions:

  • Local complement activation via classical, lectin, and alternative pathways is implicated in tubulointerstitial injury and DN progression.
  • Complement components like C3 and C1q are potential biomarkers for DN progression and renal outcomes.
Keywords:
WGCNAcomplement systemdiabetic nephropathyprognosistubulointerstitial injury

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