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Comment
. 2021 Nov;74(5):2920-2921.
doi: 10.1002/hep.32026. Epub 2021 Jul 29.

Letter to the Editor: High Mobility Group Box Protein 1 Release Is an Identified Driver of Inflammation in the Pathogenesis of Biliary Atresia

Shaojun Shi  1 , Sunrui Chen  2 , Monique M A Verstegen  1 , Qiuwei Pan  2 , Luc J W van der Laan  1
Affiliations
Comment

Letter to the Editor: High Mobility Group Box Protein 1 Release Is an Identified Driver of Inflammation in the Pathogenesis of Biliary Atresia

Shaojun Shi et al. Hepatology. 2021 Nov.
No abstract available

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Figures

FIG. 1
FIG. 1
The role of HMGB1 in pathogenic inflammation of rotavirus‐related biliary atresia. (A) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of differentially expressed genes in rotavirus infected and uninfected ICOs. (B) Toll‐like receptor (ID: hsa04620), JAK‐STAT (ID: hsa04630), and Necroptosis (ID: hsa04217) signaling pathway from KEGG indicating upregulation (red) in ICOs upon rotavirus infection. (C) Graphic model of the autocrine and paracrine actions by HMGB1 during pathogenic inflammation induced by rotavirus infection of cholangiocytes. Abbreviations: ASC, apoptosis‐associated speck‐like protein containing a C‐terminal caspase recruitment domain; Casp1, caspase 1; dsDNA, double‐stranded DNA; ESCRT, endosomal sorting complexes required for transport; GF, epidermal growth factor; HSP90, heat shock protein 90; IFN‐α/βR, interferon‐alpha/beta receptor; IFNR, interferon receptor; IP‐10, IFN‐γ‐inducible protein 10; IRF7, interferon regulatory factor 7; i‐TAC, IFN‐inducible T‐cell α chemoattractant; LPS, lipopolysaccharide; MIG, monokine induced by IFN‐gamma; MLKL, mixed lineage kinase domain‐like; mtDNA, mitochondrial DNA; MyD88, myeloid differentiation factor 88; NF‐κB, nuclear factor kappa B; NLRP3, NOD‐, LRR‐, and pyrin domain‐containing protein 3; NOD, nucleotide‐binding oligomerization domain; OATP, organic anion‐transporting peptide; PKR, protein kinase R; p‐STAT1, phosphorylated STAT1; RIPK, receptor‐interacting serine/threonine‐protein kinase; SOCS, suppressor of cytokine signaling; STAM, signal transduction adaptor molecule; ssRNA, single‐stranded RNA; TLRs, Toll‐like receptors; TRIF, TIR‐domain‐containing adapter‐inducing interferon‐β.
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Comment on

References

    1. Mohanty SK, Donnelly B, Temple H, Ortiz‐Perez A, Mowery S, Lobeck I, et al. HMGB1 release by cholangiocytes governs biliary atresia pathogenesis and correlates with increases in afflicted infants. Hepatology 2021. Feb 8. 10.1002/hep.31745. [Epub ahead of print] - DOI - PMC - PubMed
    1. Wang J, Xu Y, Chen Z, Liang J, Lin Z, Liang H, et al. Liver immune profiling reveals pathogenesis and therapeutics for biliary atresia. Cell 2020;183:1867‐1883.e26. - PubMed
    1. Chen S, Li P, Wang Y, Yin Y, de Ruiter PE, Verstegen MMA, et al. Rotavirus infection and cytopathogenesis in human biliary organoids potentially recapitulate biliary atresia development. mBio 2020;11:e01968‐20. - PMC - PubMed