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Xin, S. ; Schick, J.A.

PUFAs dictate the balance of power in ferroptosis.

Cell Calcium 110:102703 (2023)

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Open Access Green as soon as Postprint is submitted to ZB.

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Ferroptosis is an iron-dependent form of cell death triggered by dysregulation of biochemical processes that culminate in lethal lipid peroxidation. Lipid metabolism is fundamental for determining ferroptotic fate, however, the mechanisms that alter lipid components to shape ferroptosis susceptibility remains elusive. A recent article by Lin and colleagues in Nature Communications systematically analyzed phospholipid transporters (phospholipid scramblases, flippases, and floppases), and identified that the lipid flippase solute carrier family 47 member 1 (SLC47A1) functions as a regulator of lipid remodeling and promotes ferroptosis resistance. SLC47A1 is transactivated by peroxisome proliferator activated receptor alpha (PPARA). Upon ferroptosis induction, SLC47A1 upregulation inhibits DHA/DPA polyunsaturated fatty acid containing glycerophospholipids (PUFA-PLs) accumulation to block ferroptosis. Depletion of either PPARA or SLC47A1 sensitized cells to ferroptosis by favoring ACSL4-SOAT1–mediated production of polyunsaturated fatty acid containing (PUFA) cholesterol esters. Ferroptosis has been widely linked to degenerative processes and tumor suppression. These findings indicate that lipid transporters may provide yet another means by which PUFA-containing membrane lipids convey ferroptosis sensitivity.

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Publication type Article: Journal article

Document type Letter to the Editor

Corresponding Author

Keywords Ce ; Ferroptosis ; Flippase ; Lipid Remodeling ; Mufa ; Pufa ; Sfa ; Slclc47a1

ISSN (print) / ISBN 0143-4160

e-ISSN 1532-1991

Journal Cell calcium

Quellenangaben Volume: 110, Article Number: 102703

Publisher Elsevier

Publishing Place Amsterdam

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Research Unit Signaling and Translation (SAT)

Grants Helmholtz Center Munich
German Research Foundation