Department of Biology, Stanford University, CA, USA.
FEBS J. 2022 Jan;289(2):374-385. doi: 10.1111/febs.15842. Epub 2021 Apr 7.
Cysteine is a conditionally essential amino acid required for the synthesis of proteins and many important intracellular metabolites. Cysteine depletion can trigger iron-dependent nonapoptotic cell death-ferroptosis. Despite this, cysteine itself is normally maintained at relatively low levels within the cell, and many mechanisms that could act to buffer cysteine depletion do not appear to be especially effective or active, at least in cancer cells. How do we reconcile these seemingly paradoxical features? Here, we describe the regulation of cysteine and its contribution to ferroptosis and speculate about how the levels of this amino acid are controlled to govern nonapoptotic cell death.
半胱氨酸是一种条件必需氨基酸，是合成蛋白质和许多重要细胞内代谢物所必需的。半胱氨酸耗竭会触发铁依赖性非凋亡性细胞死亡——铁死亡。尽管如此，半胱氨酸本身在细胞内通常维持在相对较低的水平，并且许多可以缓冲半胱氨酸耗竭的机制似乎并不特别有效或活跃，至少在癌细胞中是这样。我们如何调和这些看似矛盾的特征呢？在这里，我们描述了半胱氨酸的调节及其对半胱氨酸和铁死亡的贡献，并推测了如何控制这种氨基酸的水平来控制非凋亡性细胞死亡。
