Evidence map›Paper›PMID 25751601›Full record

ReviewAntioxidants & redox signaling2015

The HMGB1-RAGE Inflammatory Pathway: Implications for Brain Injury-Induced Pulmonary Dysfunction.

Daniel J Weber, Yohance M Allette, David S Wilkes, Fletcher A White

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.2field-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

48 citing papers in PubMed, 69 citations in OpenAlex.

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  19. The HMGB1-RAGE axis induces apoptosis in acute respiratory distress syndrome through PERK/eIF2α/ATF4-mediated endoplasmic reticulum stress.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
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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 2 institutions in 1 country.

Daniel J Weber1 Center for Immunobiology, Indiana University School of Medicine , Indianapolis, Indiana.
Yohance M Allette3 Department of Anatomy and Cell Biology, Indiana University School of Medicine , Indianapolis, Indiana.
David S Wilkes1 Center for Immunobiology, Indiana University School of Medicine , Indianapolis, Indiana.
Fletcher A White1 Center for Immunobiology, Indiana University School of Medicine , Indianapolis, Indiana.
Indiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Indiana Medical Scientist/Engineer Training ProgramT32GM077229 · NIGMS · INDIANA UNIVERSITY INDIANAPOLIS · PI GASTON, BENJAMIN, HERBERT, BRITTNEY-SHEA · 2008 to 2022
$6.0M
The role of DAMPS in painful bladder syndromeR01DK100905 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI KHANNA, RAJESH, WHITE, FLETCHER A · 2013 to 2013
$390k
Chemokine signaling in the transition from acute to chronic painI01BX002209 · VA · RLR VA MEDICAL CENTER · PI WHITE, FLETCHER A · 2014 to 2017
–
BLRD VA I01 BX002209NIDDK NIH HHS R01 DK100905NIGMS NIH HHS T32 GM077229
6 · The paper itself

Abstract

significanceDeceased patients who have suffered severe traumatic brain injury (TBI) are the largest source of organs for lung transplantation. However, due to severely compromised pulmonary lung function, only one-third of these patients are eligible organ donors, with far fewer capable of donating lungs (∼ 20%). As a result of this organ scarcity, understanding and controlling the pulmonary pathophysiology of potential donors are key to improving the health and long-term success of transplanted lungs. RECENT ADVANCES: Although the exact mechanism by which TBI produces pulmonary pathophysiology remains unclear, it may be related to the release of damage-associated molecular patterns (DAMPs) from the injured tissue. These heterogeneous, endogenous host molecules can be rapidly released from damaged or dying cells and mediate sterile inflammation following trauma. In this review, we highlight the interaction of the DAMP, high-mobility group box protein 1 (HMGB1) with the receptor for advanced glycation end-products (RAGE), and toll-like receptor 4 (TLR4). CRITICAL ISSUES: Recently published studies are reviewed, implicating the release of HMGB1 as producing marked changes in pulmonary inflammation and physiology following trauma, followed by an overview of the experimental evidence demonstrating the benefits of blocking the HMGB1-RAGE axis. FUTURE DIRECTIONS: Targeting the HMGB1 signaling axis may increase the number of lungs available for transplantation and improve long-term benefits for organ recipient patient outcomes.

Indexed as

Brain InjuriesHMGB1 ProteinHumansLungLung InjuryLung TransplantationReceptor for Advanced Glycation End ProductsSignal TransductionToll-Like Receptor 4HMGB1 ProteinHMGB1 protein, humanReceptor for Advanced Glycation End ProductsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID25751601
PMCPMC4685484
OpenAlexW2315662306

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.