Wu Yuting, Avcilar-Kücükgöze Irem, Santovito Donato, Atzler Dorothee
Institute for Cardiovascular Prevention, Ludwig-Maximilians-Universität München, 80336 Munich, Germany.
DZHK (German Center for Cardiovascular Research), Partner Site Munich Heart Alliance, 80336 Munich, Germany.
Biomolecules. 2024 Dec 6;14(12):1557. doi: 10.3390/biom14121557.
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.
心血管疾病是全球最常见的死亡原因,约占三分之一的死亡病例。主要潜在病理是动脉粥样硬化,这是一种由血脂异常驱动的慢性炎症性疾病。免疫细胞与非免疫细胞之间的相互作用在动脉粥样硬化形成的复杂过程中至关重要。在动脉粥样硬化进展过程中,细胞内代谢途径,如氨基酸代谢,是免疫细胞功能的主要调节因素。自噬是一种重要的应激生存机制,参与维持(免疫)细胞稳态,在动脉粥样硬化发展过程中至关重要,并且受到氨基酸可用性的强烈调节。在本综述中,我们重点关注氨基酸,尤其是L-亮氨酸、L-精氨酸和L-谷氨酰胺与自噬在动脉粥样硬化发生和发展过程中的相互作用,突出潜在的治疗前景。