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Updated: Jan 23, 2026

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てんかん性神経細胞障害におけるPLA2R1を介したERK依存性フェロプトーシス：重要な病因メカニズム

Hong Chen¹, Guohang Wu², Qiannan Song³

¹Department of Pediatrics, First Affiliated Hospital, Heilongjiang University of Chinese Medicine, Heilongjiang 150040, China.

Experimental cell research

|January 21, 2026

要旨

Background:

Phospholipase A2 receptor 1 (PLA2R1) plays a regulatory role in pathological processes, but its mechanism in epileptic neuronal injury remains unclear. This study aimed to elucidate how PLA2R1 promotes epileptic neuronal injury through ERK-dependent ferroptosis.

Methods:

A kainic acid-induced epilepsy mouse model was employed. PLA2R1 expression was detected using qRT-PCR, Western blot, and immunofluorescence. PLA2R1 knockdown and overexpression vectors were constructed to observe effects on seizure severity and neuronal injury. Ferroptosis indicators (GPX4, ACSL4, PTGS2, MDA, ROS, GSH) were analyzed. HT22 cells were used for in vitro validation with glutamate and Erastin-induced ferroptosis. ERK pathway involvement was verified using inhibitor SCH772984.

Results:

PLA2R1 was upregulated in epileptic tissues. PLA2R1 knockdown prolonged seizure latency, reduced seizure intensity, decreased neuronal injury, and inhibited ERK activation. It upregulated GPX4 and GSH while downregulating ACSL4, PTGS2, MDA, and ROS. PLA2R1 overexpression exacerbated ferroptosis-related neuronal injury. In vitro experiments confirmed that ferroptosis inducers upregulated PLA2R1, while knockdown improved neuronal survival. ERK inhibitor SCH772984 reversed PLA2R1 overexpression-induced neuronal injury.

Conclusion:

This study identified the PLA2R1-MEK-ERK-ferroptosis signaling axis, suggesting that PLA2R1 contributes to neuronal ferroptosis through ERK pathway activation in epilepsy. PLA2R1's druggability and ERK inhibitors' clinical safety provide foundation for therapeutic translation.

キーワード:

ERK経路てんかんフェロプトーシス神経細胞障害 PLA2R1

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