Abstract
Functional amino acids provide great potential for treating autophagy-related diseases by regulating autophagy. The purpose of the autophagy process is to remove unwanted cellular contents and to recycle nutrients, which is controlled by many factors. Disordered autophagy has been reported to be associated with various diseases, such as cancer, neurodegeneration, aging, and obesity. Autophagy cannot be directly controlled and dynamic amino acid levels are sufficient to regulate autophagy. To date, arginine, leucine, glutamine, and methionine are widely reported functional amino acids that regulate autophagy. As a signal relay station, mammalian target of rapamycin complex 1 (mTORC1) turns various amino acid signals into autophagy signaling pathways for functional amino acids. Deficiency or supplementation of functional amino acids can immediately regulate autophagy and is associated with autophagy-related disease. This review summarizes the mechanisms currently involved in autophagy and amino acid sensing, diverse signal transduction among functional amino acids and autophagy, and the therapeutic appeal of amino acids to autophagy-related diseases. We aim to provide a comprehensive overview of the mechanisms of amino acid regulation of autophagy and the role of functional amino acids in clinical autophagy-related diseases and to further convert these mechanisms into feasible therapeutic applications.
Highlights
A delicate balance of organelle generation and renovation is required to guarantee normal differentiation and development in mammalian cells
After introducing our understanding of autophagy and the amino acid sensing mechanism briefly, this review describes the specific autophagy regulated by signal transduction of functional amino acids and the association between autophagy-related diseases and functional amino acids
We provide an overview of the impacts of amino acids with autophagy and propose the novel clinical treatment of autophagy-related diseases based on the indirect regulation of functional amino acids
Summary
A delicate balance of organelle generation and renovation is required to guarantee normal differentiation and development in mammalian cells. To maintain the intracellular metabolic balance, cells have evolved a self-degradative process, called autophagy. In response to a certain degree of the amino acid starvation, autophagy degradation promotes the release of AA to protect cells. Under the stress of nutrient deficiency or excess, amino acids can regulate autophagy via signal transduction [6]. Functional amino acids (FAAs) (e.g., arginine, leucine, glutamine, and methionine) participate in protein synthesis and homeostasis, which lead to cell signaling transduction by certain protein kinases [7]. Mammalian target of rapamycin complex 1 (mTORC1), a signal transduction regulator, links FAAs with autophagy; FAAs may hold great promise for the prevention and treatment of autophagy-related diseases [7]. We provide an overview of the impacts of amino acids with autophagy and propose the novel clinical treatment of autophagy-related diseases based on the indirect regulation of functional amino acids
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