Department of Biology, Stanford University, Stanford, CA, USA.
Department of Chemistry and Biomolecular Sciences, University of Ottawa, Ottawa, ON, Canada.
Mol Cell. 2023 Apr 6;83(7):1030-1042. doi: 10.1016/j.molcel.2023.03.005. Epub 2023 Mar 27.
It is common to think about and depict biological processes as being governed by fixed pathways with specific components interconnected by concrete positive and negative interactions. However, these models may fail to effectively capture the regulation of cell biological processes that are driven by chemical mechanisms that do not rely absolutely on specific metabolites or proteins. Here, we discuss how ferroptosis, a non-apoptotic cell death mechanism with emerging links to disease, may be best understood as a highly flexible mechanism that can be executed and regulated by many functionally related metabolites and proteins. The inherent plasticity of ferroptosis has implications for how to define and study this mechanism in healthy and diseased cells and organisms.
人们普遍认为,生物过程是由固定的途径控制的,这些途径具有特定的组成部分,通过具体的正负相互作用相互连接。然而,这些模型可能无法有效地捕捉到由化学机制驱动的细胞生物学过程的调节,而这些化学机制并不绝对依赖于特定的代谢物或蛋白质。在这里,我们讨论了铁死亡(一种与疾病有新联系的非凋亡细胞死亡机制)如何被最好地理解为一种高度灵活的机制,它可以由许多功能相关的代谢物和蛋白质来执行和调节。铁死亡的固有可塑性对如何在健康和患病细胞和生物体中定义和研究这一机制具有重要意义。