PEG out through the pores with the help of ESCRTIII
Alejandro Marmolejo-Garza1, Amalia M Dolga2
1Faculty 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.
Abstract:
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.
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