Epiandrosterone attenuates neuronal ferroptosis after subarachnoid hemorrhage by OGT-mediated FTH O-GlcNAcylation to suppress NCOA4-dependent ferritinophagy

Shengji Ma

doi:10.1016/j.freeradbiomed.2026.07.034

Epiandrosterone attenuates neuronal ferroptosis after subarachnoid hemorrhage by OGT-mediated FTH O-GlcNAcylation to suppress NCOA4-dependent ferritinophagy

2026-07-20

0

PRE

AI

S

Shengji Ma

H

Hui Yang

H

Haochen Yan

W

Wenyu Wang

C

Chen Li

B

Bingxuan Jin

J

Jiyi Li

C

Cong Yan

G

Guangyou Jiang

李慧 (Hui Li)

H

Haidong Gong

G

Guangxi Ye

N

Nan Liu *

C

Cheng Gao *

DOI：10.1016/j.freeradbiomed.2026.07.034

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• SAH induces a paradoxical discrepancy between FTH mRNA upregulation and protein downregulation. • OGT-mediated O-GlcNAcylation at FTH Serine-7 inhibits NCOA4-dependent ferritinophagy and ferroptosis. • The endogenous steroid metabolite EpiA is identified as an allosteric OGT agonist. • In vivo genetic rescue and human SH-SY5Y cell validation confirm that FTH S7 is the essential target for EpiA-mediated neuroprotection. • This study establishes the OGT–FTH axis as a therapeutic target and EpiA as a promising candidate for SAH treatment.

Epiandrosterone attenuates neuronal ferroptosis after subarachnoid hemorrhage by OGT-mediated FTH O-GlcNAcylation to suppress NCOA4-dependent ferritinophagy

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