Modulation of Glutathione Hemostasis by Inhibition of 12/15-Lipoxygenase Prevents ROS-Mediated Cell Death after Hepatic Ischemia and Reperfusion.
Moritz DrefsMichael N ThomasMarkus GubaMartin K AngeleJens WernerMarcus ConradChristian J SteibLesca M HoldtJoachim AndrassyAndrej KhandogaMarkus RentschPublished in: Oxidative medicine and cellular longevity (2017)
Our data show that inhibition of 12/15-lipoxygenase causes significant cell death reduction after hepatic ischemia and reperfusion by enhancing glutathione metabolism. We conclude that GPX4-dependent cell death signaling cascade might play a major role in development of hepatic IRI, in which the investigated proteins JNK, caspase-3, ERK1/2, and PARP might contribute to tissue damage.
Keyphrases
- cell death
- cell cycle arrest
- acute myocardial infarction
- cerebral ischemia
- dna damage
- signaling pathway
- acute ischemic stroke
- cell proliferation
- oxidative stress
- electronic health record
- mouse model
- high resolution
- atomic force microscopy
- coronary artery disease
- subarachnoid hemorrhage
- acute coronary syndrome
- induced apoptosis
- deep learning
- reactive oxygen species
- data analysis