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Advanced glycation endproducts trigger autophagy in cadiomyocyte via RAGE/PI3K/AKT/mTOR pathway

Xuwei Hou1, Zhaohui Hu, Hanying Xu

  • 1Department of Cardiology, Hangzhou Hospital, Nanjing Medical University & Hangzhou First Municipal Hospital, Hangzhou 310006, China. beckhxw007@gmail.com.

Cardiovascular Diabetology
|April 15, 2014
PubMed
Abstract

Insights

Advanced glycation end products (AGEs) trigger cardiomyocyte autophagy by inhibiting the PI3K/Akt/mTOR pathway via RAGE. This process impacts heart cell viability and function.

Area of Science:

  • Cardiovascular Biology
  • Cellular Physiology
  • Molecular Medicine

Background:

  • Advanced glycation end products (AGEs) are implicated in cardiomyocyte apoptosis and heart dysfunction.
  • The specific impact of AGEs on cardiomyocyte autophagy remains largely unexplored.

Purpose of the Study:

  • To investigate the effect of AGEs on autophagy in cardiomyocytes.
  • To elucidate the underlying molecular mechanisms involving RAGE and the PI3K/Akt/mTOR pathway.

Main Methods:

  • Primary rat neonatal cardiomyocytes were cultured and treated with varying concentrations of AGEs.
  • Western blot analysis was used to detect autophagy markers LC3 and Beclin-1.
  • Inhibition of the Receptor for AGEs (RAGE) and the PI3K/Akt/mTOR pathway was performed.

Main Results:

  • AGEs treatment dose-dependently increased Beclin-1 and LC3 II expression, autophagic vacuoles, and decreased cell viability.
  • AGEs inhibited the PI3K/Akt/mTOR pathway, mediated by RAGE.
  • RAGE inhibition reduced autophagy and reactivated the PI3K/Akt/mTOR pathway, while PI3K/Akt/mTOR inhibition abolished RAGE inhibition's protective effects.

Conclusions:

  • AGEs induce cardiomyocyte autophagy, at least partly by inhibiting the PI3K/Akt/mTOR pathway through RAGE.
  • This study reveals a novel mechanism of AGEs-induced cellular stress in cardiomyocytes.
  • Targeting the RAGE/PI3K/Akt/mTOR axis may offer therapeutic strategies for AGEs-related cardiac dysfunction.

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