Evidence map›Paper›PMID 31731454›Full record

ReviewInternational journal of molecular sciences2019

Role of High-Mobility Group Box-1 in Liver Pathogenesis.

Bilon Khambu, Shengmin Yan, Nazmul Huda, Xiao-Ming Yin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.0field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 72 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Serum HMGB1 and Alcohol-Related Liver Disease.Journal of clinical medicine · 2026
    Article
  5. Article
  6. Review
  7. Modulation of Aging Diseases via RAGE Targets: A Dietary Intervention Review.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  8. Article
  9. Article
  10. Dysbiosis and extraintestinal cancers.Journal of experimental & clinical cancer research : CR · 2025
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Bilon KhambuDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.ORCID 0000-0002-9432-2064
Shengmin YanDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.ORCID 0000-0003-4012-9557
Nazmul HudaDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.ORCID 0000-0002-7788-8621
Xiao-Ming YinDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University School of Medicine

Funding

The Role of HMGB1 in autophagy deficiency-induced liver pathologyR01DK116605 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI YIN, XIAO-MING · 2018 to 2021
$1.7M
NIDDK NIH HHS R01 DK116605
6 · The paper itself

Abstract

High-mobility group box 1 (HMGB1) is a highly abundant DNA-binding protein that can relocate to the cytosol or undergo extracellular release during cellular stress or death. HMGB1 has a functional versatility depending on its cellular location. While intracellular HMGB1 is important for DNA structure maintenance, gene expression, and autophagy induction, extracellular HMGB1 acts as a damage-associated molecular pattern (DAMP) molecule to alert the host of damage by triggering immune responses. The biological function of HMGB1 is mediated by multiple receptors, including the receptor for advanced glycation end products (RAGE) and Toll-like receptors (TLRs), which are expressed in different hepatic cells. Activation of HMGB1 and downstream signaling pathways are contributing factors in the pathogenesis of non-alcoholic fatty liver disease (NAFLD), alcoholic liver disease (ALD), and drug-induced liver injury (DILI), each of which involves sterile inflammation, liver fibrosis, ductular reaction, and hepatic tumorigenesis. In this review, we will discuss the critical role of HMGB1 in these pathogenic contexts and propose HMGB1 as a bona fide and targetable DAMP in the setting of common liver diseases.

Indexed as

Signal TransductionAnimalsHMGB1 ProteinHumansLiverLiver DiseasesReceptor for Advanced Glycation End ProductsToll-Like ReceptorsAGER protein, humanHMGB1 ProteinHMGB1 protein, humanReceptor for Advanced Glycation End ProductsToll-Like ReceptorsALDautophagyDILIductular reactionfibrosisHMGB1inflammationNAFLDtumor

Identifiers

PMID31731454
PMCPMC6862281
OpenAlexW2981816606

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.