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Glycation-induced modification of tissue-specific ECM proteins: A pathophysiological mechanism in degenerative

Sneha B Bansode1, Rajesh N Gacche1

  • 1Department of Biotechnology, Savitribai Phule Pune University, Pune 411007, India.

Biochimica Et Biophysica Acta. General Subjects
|August 11, 2019
PubMed
Abstract

Insights

Advanced glycation end products (AGEs) damage extracellular matrix (ECM) proteins, altering tissue properties and cell behavior. Understanding these glycation mechanisms is crucial for managing degenerative diseases.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pathophysiology

Background:

  • Glycation leads to advanced glycation end products (AGEs), impacting human degenerative diseases.
  • Glycation of extracellular matrix (ECM) proteins impairs tissue mechanical and functional properties.
  • Deciphering the mechanisms of glycation is essential due to its adverse pathophysiological effects.

Purpose of the Study:

  • To review AGE-induced modifications of tissue-specific ECM proteins.
  • To explore the implications of these modifications in organ-specific human ailments.
  • To provide comprehensive knowledge on ECM remodeling and glycation-induced pathology.

Main Methods:

  • Literature review of glycation mechanisms and ECM modification.
  • Analysis of AGEs' impact on protein structure-function and cell interactions.
  • Examination of signaling pathways activated by AGE-receptor interactions.

Main Results:

  • Glycated ECM proteins alter cell behavior by affecting receptor interactions (e.g., integrins).
  • AGE-modified ECM impacts matrix-matrix and matrix-cell interactions.
  • Downstream signaling pathways are affected, influencing tissue properties and disease progression.

Conclusions:

  • Glycation-induced ECM alterations contribute to the initiation and progression of degenerative diseases.
  • Understanding these processes may lead to drug development for mitigating AGE effects.
  • Novel strategies for managing glycation-induced diseases can be explored.
Keywords:
Cellular signallingDegenerative diseasesExtracellular matrixProtein glycationRAGE

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