17β-estradiol significantly inhibits the CGC and inflammation caused by TGF-β in HTFs. This inhibition is likely related to the suppression of stress fibers, inhibition of MMPs, and attenuation of Smads and MAPK (ERK and p38) signaling. 17β-estradiol may have potential clinical benefits in preventing scar development and inflammation in the conjunctiva.
Keyphrases
- signaling pathway
- transforming growth factor
- epithelial mesenchymal transition
- oxidative stress
- pi k akt
- estrogen receptor
- diabetic rats
- endothelial cells
- wound healing
- induced apoptosis
- high glucose
- drug induced
- induced pluripotent stem cells
- smooth muscle
- risk assessment
- human health
- pluripotent stem cells
- climate change