Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
April 13, 2026SHILAP Revista de lepidopterologíaOpen Access

Exosomal hsa-miR-299-3p from endothelium mediates high phosphorus-induced vascular calcification in mice model of CKD via phosphorylated JAK2/STAT5 pathway

View Full Paper
Ask AI
Bookmark
Share

Authors

SCSi-Jie ChenTTTao-Tao TangLXLi-Jun Xie

Discussion

Loading...

Member takes

Overview

Investigates exosomal miR-299-3p's role in vascular calcification in chronic kidney disease, indicating a new therapeutic target.

Key Points

  • To explore how hyperphosphatemia-induced exosomal microRNAs from endothelial cells contribute to vascular calcification in chronic kidney disease.
  • Established a CKD-VC mouse model with high phosphorus diet
  • Isolated exosomes from endothelial cells under high phosphorus conditions
  • Evaluated the effects of exosomes on vascular smooth muscle cell calcification in vitro and in vivo
  • Performed miRNA sequencing, luciferase assays, and molecular analyses
  • Conducted knockdown experiments to observe functional implications of miR-299-3p
  • High phosphorus stimulated endothelial cells released exosomes that promoted vascular calcification in VSMCs
  • miR-299-3p was significantly upregulated in exosomes from high phosphorus-stimulated endothelial cells
  • Exosomal miR-299-3p activated the p-JAK2/STAT5 pathway, promoting osteogenic differentiation
  • Knockdown of miR-299-3p reduced vascular calcification in CKD mice

Cite This Study

Chen et al. (2026) studied this question.

synapsesocial.com/papers/69dc874a3afacbeac03e9c4bhttps://doi.org/10.3389/fphar.2026.1752954
View Full Paper
Ask AI
Bookmark
Share