Post-translational modifications drive the effects of HMGB1 in alcohol-associated liver disease
These results provide evidence for targeting [O] HMGB1 of hepatocyte origin as a ligand for RAGE signaling in myeloid cells and a driver of steatosis, inflammatory cell infiltration, and IL1B production in AALD. Importantly, we reveal that [Ac] HMGB1 offsets the noxious effects of [O] HMGB1 in AALD.
Authors
- Sukanta Das (ORCID: https://orcid.org/0000-0002-2376-1174)
- Yujin Hoshida (ORCID: https://orcid.org/0000-0001-9430-1426)
- Romain Désert (ORCID: https://orcid.org/0000-0001-8786-5741)
- Chao Wang (ORCID: https://orcid.org/0000-0001-5019-2379)
- Sai Santosh Babu Komakula (ORCID: https://orcid.org/0000-0001-6109-2736)
- Xiaodong Ge (ORCID: https://orcid.org/0000-0002-6311-8837)
- Nithyananthan Subramaniyam
- Natalia Nieto
- Daniel D. Lantvit (ORCID: https://orcid.org/0009-0001-0963-8890)
- Zhuolun Song (ORCID: https://orcid.org/0000-0001-5101-3950)
- Hui Han (ORCID: https://orcid.org/0000-0002-8890-4295)
- Zhan-Biao Ge
Institutions
- University of Illinois Chicago (US)
- Jesse Brown VA Medical Center (US)
- The University of Texas Southwestern Medical Center (US)
Publication Details
- Journal
- Hepatology Communications
- Published
- 2024-10-17
- DOI
- https://doi.org/10.1097/hc9.0000000000000549
- Citations
- 1
- Primary Topic
- Advanced Glycation End Products research
- Type
- article
- Field-Weighted Citation Impact
- 0.38
Funders
- U.S. Department of Veterans Affairs
- University of Pittsburgh
- Deutsches Krebsforschungszentrum