Marmolejo-Garza Alejandro, Dolga Amalia M
Faculty of Science and Engineering, Department of Molecular Pharmacology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, 9713 AV Groningen, The Netherlands; Department of Biomedical Sciences of Cells & Systems, Section Molecular Neurobiology, Faculty of Medical Sciences, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Faculty of Science and Engineering, Department of Molecular Pharmacology, Groningen Research Institute of Pharmacy (GRIP), University of Groningen, 9713 AV Groningen, The Netherlands.
Cell Calcium. 2021 May 28;97:102422. doi: 10.1016/j.ceca.2021.102422.
Ferroptosis is a form of programmed cell death with particular hallmarks, such as oxidative stress, increased calcium fluxes, and altered cellular morphology. In ferroptosis, the disruption of plasma membrane is the step that culminates into cell death. By inducing ferroptosis with Erastin-1 and RSL3 in various human cellular models, Pedrera et al. tracked the behaviour of several hallmarks of ferroptosis and demonstrated that lipid peroxidation precedes cytosolic calcium rise and plasma membrane breakdown, which is dependent on nanopore formation. Ferroptotic cell death is inhibited by osmotically active protectants of proper size that can prevent water flux through nanopores.
铁死亡是一种具有特定特征的程序性细胞死亡形式,如氧化应激、钙通量增加和细胞形态改变。在铁死亡中,质膜的破坏是导致细胞死亡的最终步骤。通过在各种人类细胞模型中用埃拉斯汀-1和RSL3诱导铁死亡,佩德雷拉等人追踪了铁死亡的几个特征的行为,并证明脂质过氧化先于胞质钙升高和质膜破裂,而质膜破裂依赖于纳米孔的形成。适当大小的渗透活性保护剂可抑制铁死亡性细胞死亡,这些保护剂可防止水通过纳米孔流动。