This study shows that the molecular regulatory mechanism of TGF-β-induced downregulation of CYGB expression in human HSCs, leading to the loss of cellular tolerance to exogenous oxidative stress and oxidative DNA damage in activated HSCs in human NASH with advanced fibrosis. Our findings provide new insights into the relationship between CYGB expression and the pathophysiology of NASH fibrosis in the human liver.
- Predictive value of blood pressure, heart rate, and blood pressure/heart rate ratio in a Chinese subpopulation with vasovagal syncope
- Risk factors for intraoperative pressure injury in aortic surgery
- ECMO/CRRT in the treatment of critically ill SARS-CoV-2 pneumonia patients
- Regulating the ribosomal RNA production line
- New technique builds super-hard metals from nanoparticles