Amino Acid Metabolism and Autophagy in Atherosclerotic Cardiovascular Disease

Yuting Wu1, Irem Avcilar-Kücükgöze1,2, Donato Santovito1,2,3

  • 1Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München, 80336 Munich, Germany.

Biomolecules
|January 8, 2025
PubMed

Insights

Cardiovascular disease, driven by atherosclerosis, involves immune cells and amino acid metabolism. This review explores how amino acids like L-leucine regulate autophagy, impacting atherosclerosis and offering therapeutic targets.

Area of Science:

  • Immunology
  • Metabolic pathways
  • Cardiovascular research

Background:

  • Cardiovascular disease is a leading global cause of death.
  • Atherosclerosis, a chronic inflammatory disease, underlies most cardiovascular deaths.
  • Immune and non-immune cell interactions are critical in atherogenesis.

Purpose of the Study:

  • To review the role of amino acid metabolism in immune cell function during atherosclerosis.
  • To examine the regulation of autophagy by amino acids in the context of atherosclerosis.
  • To highlight potential therapeutic strategies targeting amino acid-autophagy pathways.

Main Methods:

  • Literature review focusing on molecular mechanisms.
  • Analysis of the interplay between amino acids, autophagy, and immune cells.
  • Exploration of metabolic pathways in atherogenesis.

Main Results:

  • Amino acid availability, particularly L-leucine, L-arginine, and L-glutamine, significantly influences autophagy.
  • Autophagy is a key regulator of immune cell homeostasis during atherosclerosis.
  • Dysregulated amino acid metabolism impacts autophagy, contributing to disease progression.

Conclusions:

  • Amino acids and autophagy are critical regulators in atherosclerosis development.
  • Targeting amino acid-autophagy interactions presents a promising therapeutic avenue for cardiovascular disease.
  • Further research into these pathways could lead to novel treatments for atherosclerosis.

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