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S100A12-CD36 axis: A novel player in the pathogenesis of atherosclerosis?

Jamileh Farokhzadian1, Parvin Mangolian Shahrbabaki2, Vahid Bagheri3

  • 1Nursing Research Center, Kerman University of Medical Sciences, Kerman, Iran; Department of Community Health Nursing, School of Nursing and Midwifery, Kerman University of Medical Sciences, Kerman, Iran.

Cytokine
|July 31, 2017
PubMed

Insights

S100A12 protein binds to CD36, a key player in vascular inflammation and atherosclerosis. This interaction highlights S100A12 as a potential therapeutic target for treating atherosclerosis by modulating the S100A12-CD36 axis.

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Research

Background:

  • S100A12 is a calcium-binding protein involved in inflammatory processes.
  • S100A12 interacts with RAGE and TLR4, contributing to inflammation.
  • CD36 is a scavenger receptor crucial for fatty acid transport and vascular inflammation.

Purpose of the Study:

  • To investigate the mechanisms of the S100A12-CD36 axis in atherosclerosis pathogenesis.
  • To explore S100A12 as a molecular target for therapeutic development.

Main Methods:

  • The study focuses on the molecular interactions and signaling pathways involving S100A12 and CD36.
  • Analysis of the roles of RAGE and TLR4 in regulating CD36 expression in the context of S100A12 interaction.

Main Results:

  • S100A12 has been shown to bind with high affinity to CD36.
  • RAGE and TLR4 are key regulators of CD36 expression, influenced by S100A12.

Conclusions:

  • The S100A12-CD36 axis is a significant factor in the pathogenesis of atherosclerosis.
  • Targeting the S100A12-CD36 interaction presents a promising therapeutic strategy for atherosclerosis.

Keywords:
CD36Foam cellRAGES100A12TLR4oxLDL

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