Melatonin suppresses ER stress-dependent proapoptotic effects via AMPK in bone mesenchymal stem cells during mitochondrial oxidative damage.
Chong-Xi FanJianyu FengChi TangZhengbin ZhangYingtong FengWeixun DuanMingming ZhaiZedong YanLiwen ZhuLele FengHanzhao ZhuErping LuoPublished in: Stem cell research & therapy (2020)
Our data also reveal a new, potentially therapeutic mechanism by which melatonin protects BMSCs from oxidative stress-mediated mitochondrial apoptosis, possibly by regulating the AMPK-ER stress pathway.
Keyphrases
- oxidative stress
- mesenchymal stem cells
- skeletal muscle
- diabetic rats
- dna damage
- ischemia reperfusion injury
- induced apoptosis
- electronic health record
- protein kinase
- signaling pathway
- bone mineral density
- big data
- single cell
- endoplasmic reticulum stress
- soft tissue
- dna methylation
- gene expression
- body composition
- deep learning
- postmenopausal women
- pi k akt