Liver-specific deletion of RORα aggravates diet-induced nonalcoholic steatohepatitis by inducing mitochondrial dysfunction.

The trisaccharide raffinose modulates epidermal differentiation through activation of liver X receptor.

RORα switches transcriptional mode of ERRγ that results in transcriptional repression of CYP2E1 under ethanol-exposure.

22-S-Hydroxycholesterol protects against ethanol-induced liver injury by blocking the auto/paracrine activation of MCP-1 mediated by LXRα.

RORα decreases oxidative stress through the induction of SOD2 and GPx1 expression and thereby protects against nonalcoholic steatohepatitis in mice.

RORα suppresses proliferation of vascular smooth muscle cells through activation of AMP-activated protein kinase.

Treatment of IL-18-binding protein biologics suppresses fibrotic progression in metabolic dysfunction-associated steatohepatitis

Bacterial components-driven intrahepatic CXCR5hi B cells are important population for MASH progression through inducing inflammation

Rh Antigens Immunogenicity Prediction Using in silico analysis of HLA Binding

Blockade of forkhead box protein O1 signaling alleviates primary sclerosing cholangitis-induced sarcopenia in mice model