.png){kind=icon}
.png){kind=icon}
Return
YTHDC1-mediated m6A modification of PDK1 contributes to the epithelial-mesenchymal transition in smoking-induced COPD airway remodeling through lactate-induced MTA2 K539 lactylation
.png){kind=icon}
OA
AI
Y
Q
J
Y
L
H
S
T
Q
H
Y
DOI：10.1016/j.eti.2025.104715.png)
.png){kind=icon}
.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
• YTHDC1 drives glycolytic reprogramming and EMT in airway epithelial cells. • YTHDC1 regulates PDK1 in an m6A-dependent manner, leading to lactate accumulation. • Lactylation of MTA2 at K539 is involved in the CSE-induced EMT in airway epithelial cells. • Silencing of YTHDC1 alleviates airway remodeling in experimental COPD model.
Keywords:
Cigarette smoke
COPD
YTHDC1
Glycolytic reprogramming
Lactylation
AI Summary
Key information extracted from the uploaded paper, including a brief overview, abstract, background, key highlights, visual analysis, and future outlook.
Journal
IF:
7.1
Papers:
4.0K
Citations:
1.9W
Organization
Cited Papers