The Role of Oxidative Inactivation of Phosphatase PTEN and TCPTP in Fatty Liver Disease.
Thang Nguyen HuuJiyoung ParkYing ZhangHien Duong ThanhIha ParkJin Myung ChoiHyun Joong YoonSang Chul ParkHyun Ae WooSeung-Rock LeePublished in: Antioxidants (Basel, Switzerland) (2023)
Alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) are becoming increasingly prevalent worldwide. Despite the different etiologies, their spectra and histological feature are similar, from simple steatosis to more advanced stages such as steatohepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma. Studies including peroxiredoxin knockout models revealed that oxidative stress is crucial in these diseases, which present as consequences of redox imbalance. Protein tyrosine phosphatases (PTPs) are a superfamily of enzymes that are major targets of reactive oxygen species (ROS) because of an oxidation-susceptible nucleophilic cysteine in their active site. Herein, we review the oxidative inactivation of two tumor suppressor PTPs, phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and T-cell protein tyrosine phosphatase (TCPTP), and their contribution to the pathogenicity of ALD and NAFLD, respectively. This review might provide a better understanding of the pathogenic mechanisms of these diseases and help develop new therapeutic strategies to treat fatty liver disease.
Keyphrases
- reactive oxygen species
- oxidative stress
- cell proliferation
- dna damage
- protein kinase
- pi k akt
- protein protein
- amino acid
- insulin resistance
- liver fibrosis
- machine learning
- cell death
- high fat diet
- binding protein
- deep learning
- fatty acid
- type diabetes
- ischemia reperfusion injury
- gene expression
- skeletal muscle
- diabetic rats
- copy number
- candida albicans
- high fat diet induced
- fluorescent probe
- endoplasmic reticulum stress
- case control
- molecular dynamics
- cystic fibrosis