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Advanced glycation end products accelerate arteriosclerosis after renal transplantation through the AGE/RAGE/ILK

Xuzhong Liu1, Kun Liu2, Zijie Wang1

  • 1Department of Urology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu Province 210029, China.

Experimental and Molecular Pathology
|July 27, 2015
PubMed
Abstract

Insights

Advanced glycation end products (AGEs) contribute to arteriosclerosis (AS) after kidney transplants. The AGE/RAGE/ILK pathway drives vascular smooth muscle cell to osteoblast trans-differentiation, promoting AS progression.

Area of Science:

  • Nephrology
  • Cardiovascular Biology
  • Molecular Medicine

Background:

  • The role of advanced glycation end products (AGEs) in arteriosclerosis (AS) post-kidney transplantation is not fully understood.
  • Molecular mechanisms linking AGEs to AS progression require elucidation.

Purpose of the Study:

  • To investigate the impact of AGEs on arteriosclerosis in renal transplant recipients (RTRs).
  • To explore the molecular pathways, including the AGE/RAGE/ILK signaling, involved in AGE-induced vascular changes.

Main Methods:

  • Compared histological changes and biomarker expression (α-SMA, OPN) in healthy volunteers and RTRs.
  • Analyzed AGEs, α-smooth muscle actin (α-SMA), osteopontin (OPN), and integrin-linked kinase (ILK) in rat vascular smooth muscle cells (VSMCs) treated with AGEs.
  • Investigated the role of the receptor for advanced glycation end (RAGE) and ILK in AGE-induced VSMC differentiation.

Main Results:

  • RTRs exhibited significant differences in arterial histology, serum AGEs, and α-SMA/OPN expression compared to controls.
  • AGEs induced time-dependent overexpression of OPN and ILK, with reduced α-SMA expression in rat VSMCs.
  • AGE-induced ILK overexpression was preventable by RAGE inhibition.

Conclusions:

  • Advanced glycation end products (AGEs) are implicated in arteriosclerosis development and progression following kidney transplantation.
  • The AGE/RAGE/ILK pathway mediates vascular smooth muscle cell (VSMC) to osteoblast trans-differentiation, contributing to AS.
  • Targeting the AGE/RAGE/ILK pathway may offer therapeutic strategies for post-transplant arteriosclerosis.
Keywords:
AGEsArteriosclerosisILKKidney transplantationOsteoblastRAGETrans-differentiationVSMCs

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