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S100/calgranulins EN-RAGEing the blood vessels: implications for inflammatory responses and atherosclerosis

Marion A Hofmann Bowman1, Ann Marie Schmidt

  • 1Department of Medicine, The University of Chicago, Chicago, IL, USA.

American Journal of Cardiovascular Disease
|December 27, 2011
PubMed

Insights

S100 proteins and their receptor RAGE are central to atherosclerosis, a chronic inflammatory disease. Understanding their role in plaque rupture and aortic remodeling is crucial for developing new treatments.

Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Molecular Medicine

Background:

  • Atherosclerosis is a leading cause of mortality globally.
  • It involves complex chronic inflammation regulated by cellular signaling.
  • Key cells include endothelial cells, monocytes, and smooth muscle cells.

Purpose of the Study:

  • To review the biology and function of S100 proteins.
  • To examine the role of the receptor for advanced glycation end products (RAGE) in atherosclerosis.
  • To connect S100/RAGE signaling to atherosclerosis pathogenesis, plaque rupture, and aortic remodeling.

Main Methods:

  • Literature review of S100 proteins and RAGE.
  • Analysis of cytokine and chemokine signaling pathways.
  • Focus on cellular interactions in atherosclerotic development.

Main Results:

  • S100 proteins and RAGE are implicated in the inflammatory processes of atherosclerosis.
  • Their signaling network influences key cellular players in plaque formation.
  • These molecules contribute to plaque instability and aortic wall changes.

Conclusions:

  • S100 proteins and RAGE are critical mediators in atherosclerosis.
  • Targeting the S100/RAGE axis may offer therapeutic strategies.
  • Further research is needed to fully elucidate their complex roles.

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