肺炎克雷伯菌来源EVs通过抑制SIRT1损害内皮功能

核心信息

• 论文英文标题: Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1
• 期刊: Cell Commun Signal
• 发表年份: 2025
• DOI: 10.1186/s12964-024-02002-0
• PMID/PMCID: 39800699; PMC11726972

研究概览

pn) in hypertension development has been emphasized, although the specific mechanisms have not been well understood. Bacterial extracellular vesicles (BEVs) released by Gram-negative bacteria modulate host cell functions by delivering bacterial components to host cells.

核心发现

pn significantly impaired acetylcholine-induced endothelium-dependent relaxation and increased superoxide anion production in endothelial cells in vivo.

pn EVs caused significant endothelial dysfunction, endothelial provocation, and increased blood pressure.

pn EVs reduced the levels of SIRT1 and p-eNOS and increased the levels of NOX2, COX-2, ET-1, and p53 in endothelial cells.

pn EVs on endothelial cells.

研究设计

pn EVs were purified from the bacterial suspension using ultracentrifugation and characterized by transmission electron microscopy nanoparticle tracking analysis, and EV marker expression.

Superoxide anion production was measured by confocal microscopy and HUVEC senescence was assessed by SA-β-gal activity.

SIRT1 overexpression or activator was utilized to investigate the underlying mechanisms.

Echo Biotech 角色

肺炎克雷伯菌（K.pn）即细菌囊泡分离Exosupur ES8500+ES911

关联平台: Exoomics®, Research Reagents & Tools

关联服务与能力: EV Isolation & Purification, Research Reagent / Product Supply

关联产品或试剂: Exosupur® EV Isolation/Purification Kit

参考文献

原始论文: Klebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1 Cell communication and signaling. 2025. DOI: 10.1186/s12964-024-02002-0. PMID/PMCID: 39800699; PMC11726972.