Area of research
Epidemiology · Hepatology
Research interest
Research interests include Liver Disease Diagnosis and Treatment, Liver physiology and pathology, MicroRNA in disease regulation, and Hepatitis C virus research.
Activated ATF6α is a hepatic tumour driver restricting immunosurveillance
Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis
Targeting peroxiredoxin 2 prevents hepatocarcinogenesis in metabolic liver disease models
A 5:2 intermittent fasting regimen ameliorates NASH and fibrosis and blunts HCC development via hepatic PPARα and PCK1
Targeting the liver clock improves fibrosis by restoring TGF-β signaling
Ribosomal S6 kinase 1 regulates inflammaging via the senescence secretome
Lymphotoxin beta‐activated <scp>LTBR/NIK/RELB</scp> axis drives proliferation in cholangiocarcinoma
Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumourigenesis
Aged intestinal stem cells propagate cell-intrinsic sources of inflammaging in mice
Comparison of HAV and HCV infections in vivo and in vitro reveals distinct patterns of innate immune evasion and activation
Bovine meat and milk factor protein expression in tumor‐free mucosa of colorectal cancer patients coincides with macrophages and might interfere with patient survival
Beneficial effects of intermittent fasting in NASH and subsequent HCC development are executed by concerted PPARα and PCK1 action in hepatocytes
Ribosomal S6 kinase 1 regulates ‘inflammaging’ via the senescence secretome
Combined hepatocellular-cholangiocarcinoma derives from liver progenitor cells and depends on senescence and IL-6 trans-signaling
A monoclonal antibody targeting nonjunctional claudin-1 inhibits fibrosis in patient-derived models by modulating cell plasticity
Comparison of HAV and HCV infections <i>in vivo</i> and <i>in vitro</i> reveals distinct patterns of innate immune evasion and activation
NASH limits anti-tumour surveillance in immunotherapy-treated HCC
Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH
Temporal multi-omics identifies LRG1 as a vascular niche instructor of metastasis
A human liver cell-based system modeling a clinical prognostic liver signature for therapeutic discovery
Hypoxia‐Inducible Factor 1 Alpha–Mediated RelB/APOBEC3B Down‐regulation Allows Hepatitis B Virus Persistence
Intercrypt sentinel macrophages tune antibacterial NF-κB responses in gut epithelial cells via TNF
Therapeutic Effects of Inhibition of Sphingosine-1-Phosphate Signaling in HIF-2α Inhibitor-Resistant Clear Cell Renal Cell Carcinoma
Author Correction: Auto-aggressive CXCR6+ CD8 T cells cause liver immune pathology in NASH
Epithelial cells of the intestine acquire cell-intrinsic inflammation signatures during ageing
HIF-1α and HIF-2α differently regulate tumour development and inflammation of clear cell renal cell carcinoma in mice
Inhibition of LTβR signalling activates WNT-induced regeneration in lung
Publisher Correction: Inhibition of LTβR signalling activates WNT-induced regeneration in lung
Cardiac glycosides are broad-spectrum senolytics
Hepatitis B virus-induced modulation of liver macrophage function promotes hepatocyte infection