ArticleiScience2025
Direct interaction of HMGB1 with SARS-CoV-2 facilitates its infection via RAGE-dependent endocytosis.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain.Bioelectronic medicine · 2026Review
- The redox-sensitive protein HMGB1: intracellular and extracellular roles.Experimental & molecular medicine · 2026Review
- Pilot longitudinal integrated transcriptomic-metabolomic study reveals immune and metabolic signatures in non-hospitalized healthcare workers with long COVID.Frontiers in cellular and infection microbiology · 2026Article
- Pharmacological intervention of the HMGB1-pCTS-L axis to ameliorate inflammatory diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19), has caused >770 million infections since 2020. SARS-CoV-2 outcomes are largely influenced by host immune responses. Among key mediators of innate immunity, high-mobility group box 1 (HMGB1) has gained attention for its role in inflammation during SARS-CoV-2 infection, and its levels are significantly elevated in acute and post-COVID-19 cases, correlating with disease severity. This study investigated the role of HMGB1 in COVID-19 pathogenesis. Our findings demonstrate that the SARS-CoV-2 spike protein directly interacts with HMGB1, forming an HMGB1-SARS-CoV-2 complex. This complex interacts with the receptor for advanced glycation end-products (RAGE), facilitating clathrin-mediated endocytosis and enhancing SARS-CoV-2 infection in human lung cells
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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.