In nonalcoholic steatohepatitis (NASH), HIF-1α is upregulated in hepatocytes, where it induces steatosis; however, the role of HIF-1α in macrophages under metabolic stress has not been explored.
In the present study, we aimed to investigate the role of endoplasmic reticulum stress (ERS) and its related inflammation and angiogenesis in liver fibrosis in a rat model of combined hypoxia and nonalcoholic steatohepatitis (NASH) and to confirm whether the intervention of hypoxia-inducible factor 1α (HIF1α) can improve fibrosis.
The present study aims to characterize the effect of chronic intermittent hypoxia and HIF1α on the non-alcoholic steatohepatitis (NASH) process in mice, and to explore the role of the Treg/Th17 balance in the formation of NASH inflammation and fibrosis.