Evidence map›Paper›PMID 32265930›Full record

ReviewFrontiers in immunology2020

Targeting Inflammation Driven by HMGB1.

Huan Yang, Haichao Wang, Ulf Andersson

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05874193 (A Collaborative Community Effort Using Belantamab Mafodotin in Relapsed/Refractory Myeloma), which is not on this map. Cited by 378 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
378citing papers in PubMed, 3 pooled it
47.3field-weighted citation impact, top 1% 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.

NCT05874193 phase2not yet recruitingnot on this mapstarted 2026, after this paper: background citation

A Collaborative Community Effort Using Belantamab Mafodotin in Relapsed/Refractory Myeloma

TypeinterventionalSponsorCristiana Costa Chase, DORan2026 to 2028Enrolled33ConditionsRelapsed/Refractory Multiple MyelomaArmsBelantamab mafodotin
3 · Its place in the literature

Who cites it

378 citing papers in PubMed, 3 syntheses or guidelines pooled it, 616 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Review
  6. Targeting Oxidative and Immune Dysregulation in Wound Healing via Gold Nanoparticle Conjugate Chitosan.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Article
  9. HMGB1 as a danger signal in vascular remodeling.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
    Review
  10. Article
  11. Regulated cell death-induced coagulation dysfunction in sepsis.Journal of thrombosis and thrombolysis · 2026
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  19. Review
  20. Article

318 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Huan YangBioelectronic Medicine, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Haichao WangMolecular Medicine, Feinstein Institutes for Medical Research, Manhasset, NY, United States.
Ulf AnderssonDepartment of Women's and Children's Health, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
Feinstein Institute for Medical Research · USKarolinska University Hospital · SE

Funding

Molecular Basis of Bioelectronic MedicineR35GM118182 · NIGMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI TRACEY, KEVIN J · 2016 to 2025
$7.3M
Mechanisms of Novel Herbal Therapies for Sepsis.R01AT005076 · NCCIH · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI WANG, HAICHAO · 2010 to 2023
$4.3M
Regulation of HMGB1 Release in Endotoxemia.R01GM063075 · NIGMS · NORTH SHORE UNIVERSITY HOSPITAL · PI WANG, HAICHAO · 2002 to 2020
$4.2M
NCCIH NIH HHS R01 AT005076NIGMS NIH HHS R01 GM063075NIGMS NIH HHS R35 GM118182
6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) is a highly conserved, nuclear protein present in all cell types. It is a multi-facet protein exerting functions both inside and outside of cells. Extracellular HMGB1 has been extensively studied for its prototypical alarmin functions activating innate immunity, after being actively released from cells or passively released upon cell death. TLR4 and RAGE operate as the main HMGB1 receptors. Disulfide HMGB1 activates the TLR4 complex by binding to MD-2. The binding site is separate from that of LPS and it is now feasible to specifically interrupt HMGB1/TLR4 activation without compromising protective LPS/TLR4-dependent functions. Another important therapeutic strategy is established on the administration of HMGB1 antagonists precluding RAGE-mediated endocytosis of HMGB1 and HMGB1-bound molecules capable of activating intracellular cognate receptors. Here we summarize the role of HMGB1 in inflammation, with a focus on recent findings on its mission as a damage-associated molecular pattern molecule and as a therapeutic target in inflammatory diseases. Recently generated HMGB1-specific inhibitors for treatment of inflammatory conditions are discussed.

Indexed as

AlarminsAnimalsAntigens, NeoplasmHMGB1 ProteinHumansImmunity, InnateInflammationMitogen-Activated Protein KinasesMolecular Targeted TherapySignal TransductionToll-Like Receptor 4AlarminsAntigens, NeoplasmHMGB1 ProteinMitogen-Activated Protein KinasesMOK protein, humanToll-Like Receptor 4danger signaldrug targetHMGB1inflammationRAGETLR4

Identifiers

PMID32265930
PMCPMC7099994
OpenAlexW3012314530

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.