Anomalous vascular endothelium significantly contributes to various cardiovascular diseases. VE-cadherin plays a vital role in governing the endothelial barrier. Krüppel-like factor 4(KLF4), as a transcription factor, which binds the VE-cadherin promoter and enhances its transcription. Tumor necrosis factor receptor-associated factor 7 (TRAF7) is an E3 ubiquitin ligase that has been shown to modulate the degradation of KLF4. HS can covalently modify cysteine residues on proteins through S-sulfhydration, thereby influencing the structure and functionality of the target protein. However, the role of S-sulfhydration on endothelial barrier integrity remains to be comprehensively elucidated. This study aims to investigate whether protein S-sulfhydration in the endothelium regulates endothelial integrity and its underlying mechanism.

中文翻译：

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硫化氢通过 TRAF7 S-硫酸化调节糖尿病主动脉 KLF4 的泛素化降解，改善内皮屏障功能

异常的血管内皮显着导致各种心血管疾病。 VE-钙粘蛋白在调节内皮屏障方面发挥着至关重要的作用。 Krüppel样因子4（KLF4）作为转录因子，与VE-钙粘蛋白启动子结合并增强其转录。肿瘤坏死因子受体相关因子 7 (TRAF7) 是一种 E3 泛素连接酶，已被证明可以调节 KLF4 的降解。 HS可以通过S-硫化作用共价修饰蛋白质上的半胱氨酸残基，从而影响目标蛋白质的结构和功能。然而，S-硫酸化对内皮屏障完整性的作用仍有待全面阐明。本研究旨在探讨内皮中蛋白质S-硫酸化是否调节内皮完整性及其潜在机制。