Evidence map›Paper›PMID 34150000›Full record

ArticleAmerican journal of translational research2021

CRISPLD2 attenuates pro-inflammatory cytokines production in HMGB1-stimulated monocytes and septic mice.

Sheng Zhang, Lei Pei, Jinlong Qu, Lizhu Sun, Weiwei Jiang, Wenfang Li, Zhaofen Lin, Dechang Chen

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
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  4. Genetic associations in sepsis and ARDS.Frontiers in pharmacology · 2026
    Review
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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

8 authors at 2 institutions in 1 country.

Sheng ZhangDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Lei PeiDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Jinlong QuDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Lizhu SunDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Weiwei JiangDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Wenfang LiDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Zhaofen LinDepartment of Critical Care Medicine, Changzheng Hospital, Second Military Medical University Shanghai, China.
Dechang ChenDepartment of Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine Shanghai, China.
Ruijin Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

HMGB1 has been identified as a pro-inflammatory mediator which leads to sepsis lethality. Previous studies suggested that CRISPLD2 had anti-inflammatory property and might severe as a therapeutic agent in sepsis. In the present study, we first conducted bioinformatic analysis to explore the expression profile of HMGB1 in septic survivors and non-survivors. We found that the serum HMGB1 level of septic non-survivors was significantly higher than that of septic survivors, and there was a positive correlation between CRISPLD2 and HMGB1 in mRNA expression in most of the cancer and normal tissue types, revealing a co-expression or dependency relationship between the two genes. In vitro, using cultured THP-1 cells, we confirmed that HMGB1 can induce the expression of CRISPLD2 in a time dependent manner through TLR4-dependent pathway. Given that CRISPLD2 and HMGB1 shared a wide range of time scales in gene expression and the anti-inflammatory property of CRISPLD2, we further verified that HMGB1 induced cytokines production might be partially reversed by CRISPLD2. In vivo, intravenously treatment of CRISPLD2 failed to rescue septic mice, although the serum levels of inflammatory cytokines were decreased. In conclusion, our study demonstrated that HMGB1 can act as stimuli to up-regulate the expression of CRISPLD2 in THP-1 cells, and in turn, increased CRISPLD2 can curtail HMGB1 induced pro-inflammatory cytokines production. Unfortunately, the anti-inflammatory effects of CRISPLD2 did not translate into survival benefit in mice with sepsis.

Indexed as

bioinformatics analysisCRISPLD2HMGB1inflammatory responseSepsis

Identifiers

PMID34150000
PMCPMC8205833
OpenAlexW3174455282

What OpenQuestion holds

Textmetadata
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.