ArticleFrontiers in microbiology2025
Differential profiles of autophagy and Nrf2-mediated antioxidant response in HBeAg-positive versus HBeAg-negative chronic hepatitis B patients.
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: HBeAg (hepatitis B e antigen) seroconversion is a key focus in the current treatment of chronic hepatitis B. The processes of autophagy and oxidative stress has been found to be involved in HBV replication and translation. It remains unclear whether this process plays a promotive or inhibitory role in HBeAg seroconversion. Methods: This study aims to evaluate the role of autophagy in disease progression by quantifying Beclin1 and P62 (Sequestosome 1) as indicators of autophagic activity in hepatitis B patients. Additionally, the Nrf2-Keap1 pathway (nuclear factor erythroid 2-related factor 2/Kelch-like ECH-associated protein 1) serves as a marker of antioxidant defense capacity, thereby allowing an assessment of the contribution of oxidative stress to the progression of the disease in these patients. We examined the expression patterns of these factors in peripheral blood mononuclear cells (PBMCs) and plasma from both HBeAg -positive and HBeAg-negative groups ( Results: The expression levels of Beclin1 and Keap1 were significantly increased compared to those in the HBeAg-negative group ( Conclusion: Based on our findings, we conclude that autophagy and the Nrf2-Keap1 antioxidant signaling pathway play critical roles in the process of HBeAg seroconversion in chronic hepatitis B patients. Furthermore, monitoring ALT/bilirubin dynamics (linked to autophagy/oxidative stress) may assist in treatment optimization, supporting the quest for clinical cure.
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