Evidence map›Paper›PMID 33313438›Full record

ArticleHeliyon2020

HMGB1 as a potential biomarker and therapeutic target for severe COVID-19.

Ruochan Chen, Yan Huang, Jun Quan, Jiao Liu, Haichao Wang, Timothy R Billiar, Michael T Lotze, Herbert J Zeh, Rui Kang, Daolin Tang

Open access · goldAbstract read
In one paragraph

Article in Heliyon, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
15.9field-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.

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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 149 citations in OpenAlex.

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  12. Immune aging and infectious diseases.Chinese medical journal · 2024
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46 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

10 authors at 5 institutions in 2 countries.

Ruochan ChenDepartment of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Yan HuangDepartment of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Jun QuanDepartment of Infectious Diseases, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
Jiao LiuThe Third Affiliated Hospital, Guangzhou Medical University, Guangdong 510600, China.
Haichao WangLaboratory of Emergency Medicine, North Shore University Hospital, Feinstein Institute for Medical Research, Manhasset, New York 11030, USA.
Timothy R BilliarDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15219, USA.
Michael T LotzeDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania 15219, USA.
Herbert J ZehDepartment of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA.
Rui KangDepartment of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA.
Daolin TangDepartment of Surgery, UT Southwestern Medical Center, Dallas, Texas, USA.
Central South University · CNSouthwestern Medical Center · USUniversity of Pittsburgh · USFeinstein Institute for Medical Research · USThird Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 has attracted global attention due to its rapid spread around the world with substantial morbidity and associated mortality. Severe COVID-19 can be complicated by the acute respiratory distress syndrome, sepsis and septic shock leading to death. These complications are thought to result from an overactivation of the immune system, leading to a cytokine storm syndrome associated with multiple organ failure. Here, we report that high mobility group box 1 (HMGB1), a prototypical damage-associated molecular pattern (DAMP) and a central mediator of lethal inflammation, could be a potential target for innovative therapeutic strategies for COVID-19. Serum HMGB1 in severe COVID-19 patients is elevated (189.40 ± 140.88 ng/ml). Exogenous HMGB1 induces the expression of SARS-CoV-2 entry receptor ACE2 in alveolar epithelial cells in an AGER-dependent manner. Importantly, genetic (using AGER siRNA) or pharmacological (using glycyrrhizin, chloroquine, hydroxychloroquine, and FPS-ZM1) inhibition of the HMGB1-AGER pathway blocks ACE2 expression. Thus, HMGB1 inhibitors are likewise promising drug candidates for the treatment of patients suffering from COVID-19.

Indexed as

Cell cultureCell deathCOVID-19HMGB1ImmunologyInfectious diseaseInflammationMicrobiologyVirology

Identifiers

PMID33313438
PMCPMC7720697
OpenAlexW3113136031

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.