Lactylation mediated by ACSM3 alleviates ferroptosis in diabetic kidney disease

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Lactylation mediated by ACSM3 alleviates ferroptosis in diabetic kidney disease

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Co-author 1

YIFAN WANG wongkyf@connect.hku.hk The University of Hong Kong School of Chinese Medicine Hong Kong Hong Kong, China *

Co-author 2

YONGKE YOU yongke.you@szu.edu.cn Shenzhen University General Hospital Department of Nephrology Shenzhen China -

Co-author 3

JIANBO GUO gambols@connect.hku.hk The University of Hong Kong School of Chinese Medicine Hong Kong Hong Kong, China -

Co-author 4

HAO LU luhao@connect.hku.hk The University of Hong Kong School of Chinese Medicine Hong Kong Hong Kong, China -

Co-author 5

HAIYONG CHEN haiyong@hku.hk The University of Hong Kong School of Chinese Medicine Hong Kong Hong Kong, China - The University of Hong Kong-Shenzhen Hospital Department of Chinese Medicine Shenzhen China

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Introduction

Acyl-CoA synthetase medium-chain family member 3 (ACSM3) locates on the membrane of mitochondria to catalyze fatty acids. Ferroptosis is one type of cell deaths, featured with iron-dependent phospholipid peroxidation. Lactylation is a novel post-translational modification mediated by lactate. This study aimed to determine whether ACSM3 alleviates ferroptosis in diabetic kidney disease (DKD) via lactylation process.

Methods

In vivo studies involved db/m, db/db, and db/db mice administrated with ACSM3 AAVs. For in vitro experiments, HK-2 cells treated with/without HG conditions were used. RNA sequencing of gene expression and mass spectrometry analysis of post-translational modification (PTM) were employed to investigate downstream mechanisms of ACSM3.

Results

ACSM3 expression level is significantly decreased in DKD patients, as well as in db/db mice kidney. KEGG based on the kidney RNA sequencing between db/m and db/db mice indicated that ACSM3 was negatively associated with ferroptosis. In vivo, mice overexpressing ACSM3 attenuated ferroptosis in diabetic kidney. Consistently, overexpression of ACSM3 alleviated ferroptosis under HG-treated HK-2 cells. PTM screening showed that lactylation level was significantly down-regulated in HG-treated HK-2 cells with ACSM3 over-expression. We found that histone lactylation mediated by the loss of ACSM3 promoted ferroptosis in DKD.

Conclusion

Targeting on ACSM3 and lactylation may have therapeutic potential for ferroptosis in DKD.

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