Differential cytotoxicity, ER/oxidative stress, dysregulated AMPKα signaling, and mitochondrial stress by ethanol and its metabolites in human pancreatic acinar cells.
Mukund P SrinivasanKamlesh K BhopaleAnna A CaracheoLata KaphaliaGopalakrishnan LoganathanAppakalai N BalamuruganCristiana RastelliniBhupendra S KaphaliaPublished in: Alcoholism, clinical and experimental research (2021)
EtOH and its metabolites, acetaldehyde and FAEEs, caused cytotoxicity, ER/oxidative and mitochondrial stress, and dysregulated AMPKα signaling, suggesting a key role of EtOH metabolism in the etiopathogenesis of ACP. Because oxidative EtOH metabolism is negligible in the exocrine pancreas, the pathogenesis of ACP could be attributable to the formation of FAEEs and related pancreatic acinar cell injury.
Keyphrases
- oxidative stress
- induced apoptosis
- ms ms
- endothelial cells
- skeletal muscle
- estrogen receptor
- endoplasmic reticulum
- dna damage
- cell cycle arrest
- ischemia reperfusion injury
- breast cancer cells
- single cell
- diabetic rats
- endoplasmic reticulum stress
- stress induced
- cell therapy
- induced pluripotent stem cells
- cell death
- stem cells
- signaling pathway
- heat shock
- pi k akt