Evidence map›Paper›PMID 31998291›Full record

ArticleFrontiers in immunology2019

Citrullinated Histone H3 as a Therapeutic Target for Endotoxic Shock in Mice.

Qiufang Deng, Baihong Pan, Hasan B Alam, Yingjian Liang, Zhenyu Wu, Baoling Liu, Nirit Mor-Vaknin, Xiuzhen Duan, Aaron M Williams, Yuzi Tian and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
5.0field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it, 100 citations in OpenAlex.

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  13. Acta pharmaceutica Sinica. B · 2026
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10 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

12 authors at 5 institutions in 2 countries.

Qiufang DengXiangya Hospital, Central South University, Changsha, China.
Baihong PanXiangya Hospital, Central South University, Changsha, China.
Hasan B AlamDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Yingjian LiangDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Zhenyu WuXiangya Hospital, Central South University, Changsha, China.
Baoling LiuDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Nirit Mor-VakninDivision of Infectious Diseases, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, United States.
Xiuzhen DuanDepartment of Pathology, Loyola University Medical Center, Maywood, IL, United States.
Aaron M WilliamsDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Yuzi TianXiangya Hospital, Central South University, Changsha, China.
Justin ZhangDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
Yongqing LiDepartment of Surgery, University of Michigan, Ann Arbor, MI, United States.
University of Michigan–Ann Arbor · USCentral South University · CNFirst Hospital of China Medical University · CNLoyola University Medical Center · USXiangya Hospital Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis results in millions of deaths every year, with acute lung injury (ALI) being one of the leading causes of mortality in septic patients. As neutrophil extracellular traps (NETs) are abundant in sepsis, neutralizing components of NETs may be a useful strategy to improve outcomes of sepsis. Citrullinated histone H3 (CitH3) has been recently shown to be involved in the NET formation. In this study, we demonstrate that CitH3 damages human umbilical vein endothelial cells (HUVECs) and potentiates NET formation through a positive feedback mechanism. We developed a novel CitH3 monoclonal antibody to target peptidylarginine deiminase (PAD) 2 and PAD 4 generated CitH3. In a mouse model of lethal lipopolysaccharide (LPS) induced shock, neutralizing CitH3 with the newly developed anti-CitH3 monoclonal antibody attenuates inflammatory responses, ameliorates ALI, and improves survival. Our study suggests that effectively blocking circulating CitH3 might be a potential therapeutic method for the treatment of endotoxemia.

Indexed as

AnimalsAntibodies, MonoclonalCitrullinationDisease Models, AnimalExtracellular TrapsHistonesHumansMaleMiceNeutrophilsProtein-Arginine Deiminase Type 2Protein-Arginine Deiminase Type 4Shock, SepticAntibodies, MonoclonalHistonesPadi2 protein, mousepeptidylarginine deiminase 4, mouseProtein-Arginine Deiminase Type 2Protein-Arginine Deiminase Type 4acute lung injurycitrullinated histone H3endotoxic shockinflammationneutrophil extracellular trapsnew anti-CitH3 antibodysurvival

Identifiers

PMID31998291
PMCPMC6962130
OpenAlexW2994353602

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.