Impairment of Rab7-dependent STING degradation hampers HBV replication but accelerates disease progression in chronic hepatitis B comorbid with MASLD - PubMed
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- Impairment of Rab7-dependent STING degradation hampers HBV replication but accelerates disease progression in chronic hepatitis B (CHB) comorbid with metabolic dysfunction-associated steatotic liver disease (MASLD).
- CHB-MASLD comorbidity decreases HBV replication but accelerates liver inflammation and fibrosis, linked to aberrant STING upregulation in macrophages.
- HBV synergizes with lipotoxicity to disrupt Rab7 expression and function in macrophages, impairing STING degradation via autophagic-lysosomal and endosomal-lysosomal pathways.
- Pathological STING accumulation has dual effects: cytosolic STING enhances antiviral activity and promotes inflammation, while extracellular vesicles transport STING to hepatocytes, triggering endoplasmic reticulum stress (ERS) and exacerbating injury.
- Restoring Rab7 facilitates STING degradation, attenuating pathology, and represents a novel therapeutic strategy.