Evidence map›Paper›PMID 34040166›Full record

ReviewActa pharmacologica Sinica2022

Targeting HMGB1 for the treatment of sepsis and sepsis-induced organ injury.

Chao Deng, Lin Zhao, Zhi Yang, Jia-Jia Shang, Chang-Yu Wang, Ming-Zhi Shen, Shuai Jiang, Tian Li, Wen-Cheng Di, Ying Chen and 3 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 2 pooled it
9.6field-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

84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 116 citations in OpenAlex.

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24 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

13 authors at 7 institutions in 1 country.

Chao Deng *Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Lin Zhao *Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.
Zhi Yang *Xi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Jia-Jia ShangXi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Chang-Yu WangDepartment of Cardiology, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Ming-Zhi ShenHainan Hospital of PLA General Hospital, The Second School of Clinical Medicine, Southern Medical University, Sanya, 572013, China.
Shuai JiangXi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Tian LiXi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Wen-Cheng DiNational Clinical Research Center for Infectious Diseases, Shenzhen Third People's Hospital, Southern University of Science and Technology, Shenzhen, 518100, China.
Ying ChenDepartment of Hematology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
He LiXi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China.
Ye-Dong ChengDepartment of Orthopaedics, Huaian Medical District of Jingling Hospital, Medical School of Nanjing University, Huaian, 213001, China. yedongcheng888@126.com.
Yang YangXi'an Key Laboratory of Cardiovascular and Cerebrovascular Diseases, Xi'an No.3 Hospital, School of Life Sciences and Medicine, Northwest University, Xi'an, 710021, China. yang200214yy@nwu.edu.cn.
Ministry of Education of the People's Republic of China · CNFirst Affiliated Hospital of Xi'an Jiaotong University · CNNorthwest University · CNAir Force Medical University · CNNanjing University · CNShenzhen Third People’s Hospital · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) is a ubiquitous nuclear protein that is present in almost all cells and regulates the activity of innate immune responses in both intracellular and extracellular settings. Current evidence suggests that HMGB1 plays a pivotal role in human pathological and pathophysiological processes such as the inflammatory response, immune reactions, cell migration, aging, and cell death. Sepsis is a systemic inflammatory response syndrome (SIRS) that occurs in hosts in response to microbial infections with a proven or suspected infectious etiology and is the leading cause of death in intensive care units worldwide, particularly in the aging population. Dysregulated systemic inflammation is a classic characteristic of sepsis, and suppression of HMGB1 may ameliorate inflammation and improve patient outcomes. Here, we focus on the latest breakthroughs regarding the roles of HMGB1 in sepsis and sepsis-related organ injury, the ways by which HMGB1 are released, and the signaling pathways and therapeutics associated with HMGB1. This review highlights recent advances related to HMGB1: the regulation of HMBG1 might be helpful for both basic research and drug development for the treatment of sepsis and sepsis-related organ injury.

Indexed as

AutophagyBlood Coagulation DisordersCytokine Release SyndromeEndoplasmic Reticulum StressHMGB1 ProteinHumansInflammationInflammation MediatorsMitochondriaMultiple Organ FailureReceptor for Advanced Glycation End ProductsSepsisSignal TransductionToll-Like ReceptorsHMGB1 ProteinInflammation MediatorsReceptor for Advanced Glycation End ProductsToll-Like Receptorshigh mobility group box 1inflammationLPSsepsisToll-like receptor

Identifiers

PMID34040166
PMCPMC8888646
OpenAlexW3165476197

What Socratic 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 Socratic graph.