Small molecule HCY-NBD stabilizes GSTM2 via cys174 sulfenylation to attenuate high glucose induced endothelial cell senescence and calcification.

Yangyang Zhang, Xinyu Dong, Xiaomeng Yan, Congyao Zhao, Xiaohui Chi, Baoxiang Zhao, Junying Miao, Fanzhen Hong, Zhaomin Lin

Shandong Provincial Key Laboratory of Development and Regeneration, School of Life Science, Shandong University, Qingdao, 266237, PR China. Electronic address: [email protected] Provincial Key Laboratory of Development and Regeneration, School of Life Science, Shandong University, Qingdao, 266237, PR China. Electronic address: [email protected]. · pubmed

Paper

Abstract

Exogenous Glutathione S-transferase Mu 2 (GSTM2) supplementation has emerged as a promising strategy to counteract aging. However, approaches to enhance endogenous GSTM2 expression remain underexplored. Here, we identify HCY-NBD, an SO

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Research summary

The paper claims that HCY-NBD stabilizes GSTM2 through cys174 sulfenylation, which attenuates high glucose-induced endothelial cell senescence and calcification. This research addresses a mechanism related to aging by exploring ways to enhance endogenous GSTM2 expression, which could have implications for age-related cellular senescence and vascular health.

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