Synapse
⌘+K
Synapse
PulseExploreJournal ClubResearchersJournals
Instagram
HomeJournal ClubExplore
June 20, 2026Current Research in ToxicologyOpen Access

CC16 alleviates PM2.5-induced airway inflammation in asthmatic mice by targeting the E-cadherin-mediated ferroptosis regulatory axis

View Full Paper
Ask AI
Bookmark
Share

Authors

WAWang AiliSYShuo YangFXFang Xu

Discussion

Loading...

Member takes

Overview

Randomized trial demonstrates CC16 alleviates airway inflammation in asthmatic mice, suggesting new therapeutic targets.

Key Points

  • Investigate the mechanism by which CC16 protects against PM2.5-induced airway inflammation through E-cadherin-mediated ferroptosis.
  • Established PM2.5-intervened asthmatic models in C57BL/6 J mice and TC-1 cells.
  • Used quantitative proteomics and bioinformatics to identify E-cadherin's role.
  • Conducted molecular docking, Co-IP, and pull-down assays to confirm CC16-E-cadherin interaction.
  • PM2.5 exposure reduced E-cadherin levels and increased epithelial ferroptosis, while CC16 restored E-cadherin expression.
  • CC16 intervention elevated NRF2, GPX4, and SLC7A11 expression, suppressed ACSL4, and decreased lipid peroxidation.
  • CDH1 knockdown negated CC16's protective effects against ferroptosis and airway injury.

Cite This Study

Aili et al. (2026) studied this question.

synapsesocial.com/papers/6a36306fdb0793dc1a5379e1https://doi.org/10.1016/j.crtox.2026.100310
View Full Paper
Ask AI
Bookmark
Share