Evidence map›Paper›PMID 31379812›Full record

ReviewFrontiers in immunology2019

Johnny on the Spot-Chronic Inflammation Is Driven by HMGB1.

Carolina M Gorgulho, Graziela G Romagnoli, Rosh Bharthi, Michael T Lotze

Open access · goldAbstract readReview
In one paragraph

Review 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 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
6.7field-weighted citation impact, top 2% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  15. Role of microRNA-129 in cancer and non-cancerous diseases (Review).Experimental and therapeutic medicine · 2021
    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

4 authors at 3 institutions in 2 countries.

Carolina M GorgulhoTumor Immunology Laboratory, Department of Microbiology and Immunology, Botucatu Institute of Biosciences, São Paulo State University, Botucatu, Brazil.
Graziela G RomagnoliTumor Immunology Laboratory, Department of Microbiology and Immunology, Botucatu Institute of Biosciences, São Paulo State University, Botucatu, Brazil.
Rosh BharthiDAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, United States.
Michael T LotzeDAMP Laboratory, Department of Surgery, Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, United States.
Universidade Estadual Paulista (Unesp) · BRUniversity of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although much has been made of the role of HMGB1 acting as an acute damage associated molecular pattern (DAMP) molecule, prompting the response to tissue damage or injury, it is also released at sites of chronic inflammation including sites of infection, autoimmunity, and cancer. As such, the biology is distinguished from homeostasis and acute inflammation by the recruitment and persistence of myeloid derived suppressor cells, T regulatory cells, fibrosis and/or exuberant angiogenesis depending on the antecedents and the other individual inflammatory partners that HMGB1 binds and focuses, including IL-1β, CXCL12/SDF1, LPS, DNA, RNA, and sRAGE. High levels of HMGB1 released into the extracellular milieu and its persistence in the microenvironment can contribute to the pathogenesis of many if not all autoimmune disorders and is a key factor that drives inflammation further and worsens symptoms. HMGB1 is also pivotal in the maintenance of chronic inflammation and a "wound healing" type of immune response that ultimately contributes to the onset of carcinogenesis and tumor progression. Exosomes carrying HMGB1 and other instructive molecules are released and shape the response of various cells in the chronic inflammatory environment. Understanding the defining roles of REDOX, DAMPs and PAMPs, and the host response in chronic inflammation requires an alternative means for positing HMGB1's central role in limiting and focusing inflammation, distinguishing chronic from acute inflammation.

Indexed as

AlarminsAutoimmune DiseasesChronic DiseaseExosomesHMGB1 ProteinHumansInfectionsInflammationMyeloid-Derived Suppressor CellsNeoplasmsAlarminsHMGB1 Proteinautoimmunityautophagycancerchronic inflammationHMGB1

Identifiers

PMID31379812
PMCPMC6660267
OpenAlexW2961164265

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.