Key result
Amino acid metabolism regulates autophagy to drive atherosclerosis development and progression.
This review highlights the mechanistic importance of amino acid metabolism and autophagy in atherosclerosis, suggesting potential new therapeutic targets.
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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Wu et al. (2024) conducted a review in Atherosclerotic Cardiovascular Disease. Amino acids (L-leucine, L-arginine, and L-glutamine) was evaluated. Amino acid metabolism, particularly involving L-leucine, L-arginine, and L-glutamine, strongly regulates autophagy and plays a crucial role in the development and progression of atherosclerosis.
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