What question did this study set out to answer?

To explore how LGALS3 induces ferroptosis through autophagy in the context of vascular calcification in chronic kidney disease (CKD).

March 28, 2026Kidney International Reports0 citationsOpen Access

WCN26-5527 LGALS3 induces ferroptoisis via interaction of autophagy in CKD vascular calcification

LHLiming HuangUniversity of Electronic Science and Technology of China GLGuoli Li YLYi LiHohai University

Key Points

To explore how LGALS3 induces ferroptosis through autophagy in the context of vascular calcification in chronic kidney disease (CKD).
Analyzed the interaction of LGALS3 with autophagy pathways.
Examined the role of BRG1 and ABHD17 in vascular smooth muscle cells (VSMCs).
Investigated the effects of protein S-palmitoylation on vascular calcification.
Identified ABHD17B as a potential target for preventing vascular calcification.
Demonstrated that the Cys1205 residue of BRG1 plays a key role in modulating procalcification effects.
Found a strong correlation between protein S-palmitoylation and vascular calcification in CKD.

Abstract

Interestingly, the Cys1205 residue of BRG1 is involved in the interaction between ABHD17 and BRG1 and affects its synergistic procalcification effect on VSMCs.Conclusion: Protein S-palmitoylation modification is closely associated with vascular calcification in CKD, and ABHD17B might be a novel potential target for the prevention and treatment of vascular calcification in CKD.I have potential conflict of interest to disclose.

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