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Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.

期刊: Cardiovascular research 日期: 2026-06-26 PMID: 42126087 浏览: 39
作者: Guo, Zhang, Shu, Xu, Zhou, Gao, Guo, Fan, Yang
Guo, Zhang, Shu, Xu, Zhou, Gao, Guo, Fan, & Yang (2026). Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.. Cardiovascular research.
Guo, Zhang, Shu, Xu, Zhou, Gao, et al. Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.. Cardiovascular research. 2026; PMID: 42126087
Guo, Zhang, Shu, et al. Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.[J]. Cardiovascular research. 2026.
@article{guo2026,
  author = {Guo and Zhang and Shu and Xu and Zhou and Gao and Guo and Fan and Yang},
  title = {Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.},
  journal = {Cardiovascular research},
  year = {2026},
  note = {PMID: 42126087},
}
TY  - JOUR
AU  - Guo
AU  - Zhang
AU  - Shu
AU  - Xu
AU  - Zhou
AU  - Gao
AU  - Guo
AU  - Fan
AU  - Yang
TI  - Histone H3 lysine 18 lactylation-mediated SULF1 transcription promotes atherosclerosis by regulating endothelial-to-mesenchymal transition.
T2  - Cardiovascular research
PY  - 2026
AN  - PMID:42126087
ER  - 

摘要

Endothelial-to-mesenchymal transition (EndMT) has emerged as a pathophysiological process responsible for various chronic vascular diseases, particularly atherosclerosis. However, the molecular pathways that govern EndMT are poorly defined. This study aimed to investigate whether sulfatase-1 (SULF1) plays a role in oxidative stress-induced EndMT and atherosclerosis.

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