ArticleCellular & molecular immunology2022
STING signaling activation inhibits HBV replication and attenuates the severity of liver injury and HBV-induced fibrosis.
Article in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Molecular mechanisms and therapeutic strategies of cGAS-STING pathway in liver disease: the quest continues.Frontiers in immunology · 2025Pooled it
- Dual HBV cccDNA-linked HiBiT reporter hepatocyte models for screening of candidate cccDNA modulators.Virulence · 2026Article
- Comparative innate immune responses across major RNA and DNA viral infections: Mechanisms, immunopathology, and therapeutic perspectives.Human vaccines & immunotherapeutics · 2026Review
- The Significance of cGAS-STING Signaling in Response to Oncogenic Viruses.Cell biochemistry and function · 2026Review
- Identification of Promising Candidate Genes and Immune Infiltration Patterns in Chronic Schistosomiasis-Associated Liver Injury by WGCNA and Machine Learning.Pathogens (Basel, Switzerland) · 2026Article
- AURKA regulates HBV-induced hepatic stellate cell inflammation and liver fibrosis by modulating K48-linked ubiquitination and proteasomal degradation of TLR3.Journal of bioenergetics and biomembranes · 2026Article
- Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026Review
- Roles of the cGAS-STING signaling pathway in viral latency.Journal of virology · 2026Review
- STING agonists as antiviral agents.FEBS letters · 2026Review
- Innate immune recognition and evasion strategies of hepatitis B virus: from DNA to RNA and viral proteins.Frontiers in immunology · 2026Review
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- Antiviral and immune modulatory activities of STING agonists in a mouse model of persistent hepatitis B virus infection.PLoS pathogens · 2025Article
- The lignan compound matairesinol monoglucoside induces type I interferon production in HBV infection immunity by regulating STING signaling.RSC medicinal chemistry · 2025Article
- Histopathological Features and Antiviral Efficacy in Patients Over 30 Years Old with Chronic Hepatitis B in the Indeterminate Phase.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- The role of liver macrophages in viral liver pathogenesis.Journal of leukocyte biology · 2025Review
- HBV infection upregulates GP73 expression to promote liver fibrosis by enhancing ER stress via the Smad2 pathway.Immunologic research · 2025Article
- Progress Update on STING Agonists as Vaccine Adjuvants.Vaccines · 2025Review
- Universal STING Pathway-Activating Complexes Counteract Viral Immune Evasion and Boost Antiviral Responses.ACS nano · 2025Article
- Hepatitis B virus confers innate immunity evasion through hepatitis B virus-miR-3 down-regulation of cGAS-Sting-IFN signaling.World journal of hepatology · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The covalently closed circular DNA (cccDNA) of HBV plays a crucial role in viral persistence and is also a risk factor for developing HBV-induced diseases, including liver fibrosis. Stimulator of interferon genes (STING), a master regulator of DNA-mediated innate immune activation, is a potential therapeutic target for viral infection and virus-related diseases. In this study, agonist-induced STING signaling activation in macrophages was revealed to inhibit cccDNA-mediated transcription and HBV replication via epigenetic modification in hepatocytes. Notably, STING activation could efficiently attenuate the severity of liver injury and fibrosis in a chronic recombinant cccDNA (rcccDNA) mouse model, which is a proven suitable research platform for HBV-induced fibrosis. Mechanistically, STING-activated autophagic flux could suppress macrophage inflammasome activation, leading to the amelioration of liver injury and HBV-induced fibrosis. Overall, the activation of STING signaling could inhibit HBV replication through epigenetic suppression of cccDNA and alleviate HBV-induced liver fibrosis through the suppression of macrophage inflammasome activation by activating autophagic flux in a chronic HBV mouse model. This study suggests that targeting the STING signaling pathway may be an important therapeutic strategy to protect against persistent HBV replication and HBV-induced fibrosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.