An advanced glycation end product (AGE)-receptor for AGEs (RAGE) axis restores adipogenic potential of senescent

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Updated: May 16, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

Chih-Yu Chen1, Allison Martorano Abell, Yang Soo Moon

  • 1Department of Food Science, Purdue University, West Lafayette, Indiana 47906, USA.

The Journal of Biological Chemistry
|November 15, 2012
PubMed

Insights

Advanced glycation end products (AGEs) promote fat cell formation in aging preadipocytes by activating the receptor for AGE (RAGE) pathway. This AGE-RAGE interaction impacts p53 function, offering new insights into diet-related aging of adipose tissue.

Area of Science:

  • Cellular biology
  • Aging research
  • Metabolic disease

Background:

  • Adipose tissue aging is characterized by impaired adipogenesis in senescent preadipocytes.
  • Advanced glycation end products (AGEs) are implicated in aging and related diseases, but their role in adipose aging is unclear.

Purpose of the Study:

  • To investigate the role of AGEs in the adipogenic potential of senescent preadipocytes.
  • To elucidate the underlying molecular mechanisms involving the receptor for AGE (RAGE) and p53.

Main Methods:

  • Utilized glycated bovine serum albumin (BSA) as a model AGE in vitro and ex vivo.
  • Assessed adipogenesis in senescent and non-senescent preadipocytes and mouse embryonic fibroblasts.
  • Examined the expression and function of RAGE, p53, and p21.
  • Investigated RAGE-p53 binding.

Main Results:

  • AGEs, specifically glycated BSA, restored impaired adipogenesis in senescent preadipocytes but not in non-senescent ones.
  • AGE-induced RAGE expression was essential for this pro-adipogenic effect.
  • RAGE mediated the impairment of p53 expression and its regulatory function on p21 in senescent cells.
  • Direct binding between RAGE and p53 was observed.

Conclusions:

  • The AGE-RAGE axis has a novel pro-adipogenic function in senescent preadipocytes.
  • This pathway influences p53-regulated adipogenesis, impacting aging-related adipose dysfunction.
  • Findings provide insights into how dietary or endogenous AGEs contribute to aging-dependent adiposity.

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