What question did this study set out to answer?

This research aims to clarify the relationship between autophagy and ferroptosis, focusing on how these processes affect ACSL3 in cerebral ischemia-reperfusion injury.

August 11, 2026Antioxidants and Redox Signaling

Dual Regulation of ACSL3 by TRIM33-Mediated Ubiquitination and NBR1-Dependent Autophagy: A Therapeutic Target for Cerebral Ischemia-Reperfusion Injury

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This research aims to clarify the relationship between autophagy and ferroptosis, focusing on how these processes affect ACSL3 in cerebral ischemia-reperfusion injury.
Conducted oxygen-glucose deprivation/reperfusion experiments in PC12 cells and middle cerebral artery occlusion (MCAO) in rats.
Utilized molecular, pharmacological, and imaging techniques to analyze ACSL3 regulation.
Administered curcumin derivative 5g and ferroptosis inhibitor Ferfluor-1 to evaluate functional recovery.
Ischemia-reperfusion significantly increased autophagy and led to ACSL3 degradation via NBR1, promoting ferroptosis.
TRIM33 ubiquitinates ACSL3, enhancing its proteasomal degradation in ischemic conditions.
CUR5g treatment restored ACSL3 levels and improved functional recovery in MCAO rats (specific metrics not provided).

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Implication

Randomized trial examines the role of autophagy and TRIM33 in regulating ACSL3 in ischemic stroke, suggesting intervention strategies.

Cite This Study

Yang et al. (2026) studied this question.

synapsesocial.com/papers/6a7ace3e3401087f2249e22b https://doi.org/10.1177/15230864261470736

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Dual Regulation of ACSL3 by TRIM33-Mediated Ubiquitination and NBR1-Dependent Autophagy: A Therapeutic Target for Cerebral Ischemia-Reperfusion Injury

Key Points

Discussion

Implication

Cite This Study

Dual Regulation of ACSL3 by TRIM33-Mediated Ubiquitination and NBR1-Dependent Autophagy: A Therapeutic Target for Cerebral Ischemia-Reperfusion Injury

Key Points

Discussion

Implication

Cite This Study

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