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Inhibition of complement system-related gene ITGB2 attenuates epithelial-mesenchymal transition and inflammation in

Jun Peng1, Wenqi Zhao2, Lu Zhou2

  • 1Nephrology Department, Central Theater Command General Hospital of the Chinese People's Liberation Army, No.627, Wuluolu, Wuchang District, Wuhan, 430070, Hubei, China. 30832644@qq.com.

European Journal of Medical Research
|February 7, 2025
PubMed
Abstract

Insights

The complement system plays a role in diabetic nephropathy (DN). This study identified ITGB2 as a key biomarker, finding that inhibiting ITGB2 reduces inflammation and epithelial-mesenchymal transition in DN.

Area of Science:

  • Immunology
  • Nephrology
  • Genomics

Background:

  • The complement system is implicated in the development of diabetic nephropathy (DN).
  • Identifying key biomarkers is crucial for understanding DN pathogenesis and developing targeted therapies.

Purpose of the Study:

  • To explore complement system-related key biomarkers in patients with diabetic nephropathy (DN).
  • To investigate the role of identified biomarkers in DN progression and potential therapeutic targets.

Main Methods:

  • Utilized microarray datasets from the GEO database to identify differentially expressed genes (DEGs) in DN.
  • Employed Weighted Gene Co-expression Network Analysis (WGCNA) and machine learning algorithms to screen for complement system-related genes (CSRGs) and identify key biomarkers.
  • Conducted in vitro experiments using high-glucose-treated HK-2 cells to validate the role of ITGB2, including assessing cell viability, inflammatory markers, and epithelial-mesenchymal transition (EMT) and fibrosis markers.

Main Results:

  • Identified 13 differential complement system-related genes (DCSRGs) and pinpointed VWF and ITGB2 as key biomarkers through machine learning.
  • VWF and ITGB2 were significantly correlated with immune cell infiltration (mast cells, NK cells, macrophages) and clinical features of DN (age, serum creatinine, GFR).
  • ITGB2 was overexpressed in high-glucose-treated HK-2 cells, and its inhibition reversed high-glucose-induced changes in cell viability, inflammation, and EMT/fibrosis markers.

Conclusions:

  • The complement system-related gene ITGB2 is overexpressed in diabetic nephropathy (DN).
  • Inhibition of ITGB2 demonstrated a protective effect by attenuating epithelial-mesenchymal transition (EMT) and inflammation in DN models.
  • ITGB2 represents a potential therapeutic target for managing diabetic nephropathy.
Keywords:
Complement systemDiabetic nephropathyImmune infiltrationMachine learningWeighted correlation network analysis

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