Evidence map›Paper›PMID 31378956›Full record

ReviewScandinavian journal of immunology2019

Decoding inflammation, its causes, genomic responses, and emerging countermeasures.

Jacek Hawiger, Jozef Zienkiewicz

Abstract readReview
In one paragraph

Review in Scandinavian journal of immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Advances and transgressions of nuclear transport checkpoint inhibitors.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  11. Review
  12. Review
  13. Solidagenone fromPharmaceuticals (Basel, Switzerland) · 2024
    Article
  14. Review
  15. Article
  16. Effects ofPlants (Basel, Switzerland) · 2023
    Article
  17. The homeostatic function of Regnase-2 restricts neuroinflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  18. Article
  19. Article
  20. Article
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

2 authors.

Jacek HawigerImmunotherapy Program at Vanderbilt University School of Medicine, Nashville, TN, USA.ORCID https://orcid.org/0000-0003-2721-6859
Jozef ZienkiewiczImmunotherapy Program at Vanderbilt University School of Medicine, Nashville, TN, USA.

Funding

Immunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5M
Superantigen-Induced Vascular Injury and DICR01HL069452 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2001 to 2011
$3.3M
Intracellular Therapeutics for Inflammatory Liver InjuryR01AA015752 · NIAAA · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2007 to 2011
$1.7M
Targeted Suppression of Cytokine Signaling in the Acute Phase ResponseR01HL085833 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2008 to 2011
$1.5M
Harnessing B lymphocytes as Antigen-Specific Regulators of Islet ToleranceK08DK090146 · NIDDK · VANDERBILT UNIVERSITY · PI MOORE, DANIEL J. · 2011 to 2013
$434k
Suppression of Inflammation by Intracellular Targeting of MyD88F32HL099140 · NHLBI · VANDERBILT UNIVERSITY · PI HUTCHENS, MARTHA A. · 2010 to 2011
$95k
Intracellular Protein Therapy with SOCS1 to Inhibit Acute Lung InflammationF32HL087531 · NHLBI · VANDERBILT UNIVERSITY · PI DIGIANDOMENICO, ANTONIO · 2007 to 2008
$88k
SARM-Mediated Nuclear Signaling in Innate ImmunityF32HL084214 · NHLBI · VANDERBILT UNIVERSITY · PI SETHMAN, CHAD R. · 2005 to 2005
$48k
Regulation of Innate Immunity and Inflammation Through Nuclear ReprogrammingI01BX002750 · VA · VETERANS HEALTH ADMINISTRATION · PI HAWIGER, JACK J · 2016 to 2024
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BLRD VA I01 BX002750NHLBI NIH HHS F32 HL084214NHLBI NIH HHS F32 HL087531NHLBI NIH HHS F32 HL099140NHLBI NIH HHS R01 HL069452NHLBI NIH HHS R01 HL085833NHLBI NIH HHS T32 HL069765NIAAA NIH HHS R01 AA015752NIDDK NIH HHS K08 DK090146US Department of Veterans' Affairs BX002750
6 · The paper itself

Abstract

Inflammation is the mechanism of diseases caused by microbial, autoimmune, allergic, metabolic and physical insults that produce distinct types of inflammatory responses. This aetiologic view of inflammation informs its classification based on a cause-dependent mechanism as well as a cause-directed therapy and prevention. The genomic era ushered in a new understanding of inflammation by highlighting the cell's nucleus as the centre of the inflammatory response. Exogenous or endogenous inflammatory insults evoke genomic responses in immune and non-immune cells. These genomic responses depend on transcription factors, which switch on and off a myriad of inflammatory genes through their regulatory networks. We discuss the transcriptional paradigm of inflammation based on denying transcription factors' access to the nucleus. We present two approaches that control proinflammatory signalling to the nucleus. The first approach constitutes a novel intracellular protein therapy with bioengineered physiologic suppressors of cytokine signalling. The second approach entails control of proinflammatory transcriptional cascades by targeting nuclear transport with a cell-penetrating peptide that inhibits the expression of 23 out of the 26 mediators of inflammation along with the nine genes required for metabolic responses. We compare these emerging anti-inflammatory countermeasures to current therapies. The transcriptional paradigm of inflammation offers nucleocentric strategies for microbial, autoimmune, metabolic, physical and other types of inflammation afflicting millions of people worldwide.

Indexed as

Disease SusceptibilityHost-Pathogen InteractionsAnimalsBiomarkersDisease ManagementGene Expression RegulationGenomicsHumansInflammationMetabolic Networks and PathwaysMolecular Targeted TherapySignal TransductionBiomarkersallergyatherosclerosisautoimmunitydiabetesgenomehepatitislung inflammationmetabolic syndromenuclear transporttranscriptiontrauma

Identifiers

PMID31378956
PMCPMC6883124

What OpenQuestion holds

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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.