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Updated: Jun 3, 2025

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
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.
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.
Abstract:
Cardiovascular disease is the most common cause of mortality globally, accounting for approximately one out of three deaths. The main underlying pathology is atherosclerosis, a dyslipidemia-driven, chronic inflammatory disease. The interplay between immune cells and non-immune cells is of great importance in the complex process of atherogenesis. During atheroprogression, intracellular metabolic pathways, such as amino acid metabolism, are master switches of immune cell function. Autophagy, an important stress survival mechanism involved in maintaining (immune) cell homeostasis, is crucial during the development of atherosclerosis and is strongly regulated by the availability of amino acids. In this review, we focus on the interplay between amino acids, especially L-leucine, L-arginine, and L-glutamine, and autophagy during atherosclerosis development and progression, highlighting potential therapeutic perspectives.
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