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- W4297007041 abstract "The discovery of regulated necrosis revitalizes the understanding of necrosis from a passive and accidental cell death to a highly coordinated and genetically regulated cell death routine. Since the emergence of RIPK1 (receptor-interacting protein kinase 1)-RIPK3-MLKL (mixed lineage kinase domain-like) axis-mediated necroptosis, various other forms of regulated necrosis, including ferroptosis and pyroptosis, have been described, which enrich the understanding of pathophysiological nature of diseases and provide novel therapeutics. Micronutrients, vitamins, and minerals, position centrally in metabolism, which are required to maintain cellular homeostasis and functions. A steady supply of micronutrients benefits health, whereas either deficiency or excessive amounts of micronutrients are considered harmful and clinically associated with certain diseases, such as cardiovascular disease and neurodegenerative disease. Recent advance reveals that micronutrients are actively involved in the signaling pathways of regulated necrosis. For example, iron-mediated oxidative stress leads to lipid peroxidation, which triggers ferroptotic cell death in cancer cells. In this review, we illustrate the crosstalk between micronutrients and regulated necrosis, and unravel the important roles of micronutrients in the process of regulated necrosis. Meanwhile, we analyze the perspective mechanism of each micronutrient in regulated necrosis, with a particular focus on reactive oxygen species (ROS)." @default.
- W4297007041 created "2022-09-25" @default.
- W4297007041 creator A5018582701 @default.
- W4297007041 creator A5020670504 @default.
- W4297007041 creator A5026798672 @default.
- W4297007041 creator A5030611214 @default.
- W4297007041 creator A5049269712 @default.
- W4297007041 creator A5054352845 @default.
- W4297007041 creator A5071798264 @default.
- W4297007041 date "2022-09-23" @default.
- W4297007041 modified "2023-10-11" @default.
- W4297007041 title "Crosstalk between regulated necrosis and micronutrition, bridged by reactive oxygen species" @default.
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