Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
June 11, 2026Chinese Medical Journal - Pulmonary and Critical Care MedicineOpen Access

UBE2M deficiency in alveolar macrophages promotes emphysema through HIF-2α/MMP12 axis

View Full Paper
Ask AI
Bookmark
Share

Authors

ZLZhouyang LiSecond Affiliated Hospital of Zhejiang UniversityDGDongyu GuoSecond Affiliated Hospital of Zhejiang UniversityYWYong WangJinan University

Discussion

Loading...

Member takes

Overview

Randomized trial investigates the UBE2M-HIF-2α-MMP12 relationship in COPD, suggesting new treatment pathways.

Key Points

  • This study aims to explore the role of protein neddylation in the pathogenesis of COPD and its therapeutic potential.
  • Assessed neddylation pathway in macrophages from COPD patients and CS-exposed mice.
  • Generated UBE2M-conditional knockout mice to study emphysema development.
  • Conducted transcriptomic profiling and pharmacological inhibition to delineate underlying mechanisms.
  • UBE2M deficiency in macrophages caused spontaneous emphysema, with increased lung volume and alveolar destruction.
  • Transcriptomic profiling identified MMP12 as a key mediator in emphysema due to UBE2M's role.
  • HIF-2α stabilization from UBE2M deficiency led to increased MMP12 expression, contributing to disease progression.

Cite This Study

Li et al. (2026) studied this question.

synapsesocial.com/papers/6a2a4fa380c8f91e7f39c8d4https://doi.org/10.1016/j.pccm.2026.05.004
View Full Paper
Ask AI
Bookmark
Share