Evidence mapPaperPMID 33245371Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2021

Burn injury induces elevated inflammatory traffic: the role of NF-κB.

Benu George, T V Suchithra, Nitish Bhatia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. [Research progress on the roles of mitochondrial fusion, fission, and mitophagy in burn wound healing​].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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  12. [Research advances on mental disorders in patients with extensive burns].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023
    Article
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  19. Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021
    Review
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

3 authors at 2 institutions in 1 country.

Benu GeorgeSchool of Biotechnology, National Institute of Technology Calicut, Kozhikode, 673601, India.
T V SuchithraSchool of Biotechnology, National Institute of Technology Calicut, Kozhikode, 673601, India.
Nitish BhatiaDepartment of Pharmacology, Khalsa College of Pharmacy, Amritsar, 143001, India. nitishnitish_18@yahoo.com.ORCID http://orcid.org/0000-0001-9606-0419
National Institute of Technology Calicut · INGovernment Medical College, Amritsar · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A burn insult generally sustains a hypovolemic shock due to a significant loss of plasma from the vessels. The burn injury triggers the release of various mediators, such as reactive oxygen species (ROS), cytokines, and inflammatory mediators. Damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), stemming from foreign microbial discharge and damaged tissue or necrotic cells from the burn-injured site, enter the systemic circulation, activate toll-like receptors (TLRs), and trigger the excessive secretion of cytokines and inflammatory mediators. Inflammation plays a vital role in remodeling an injured tissue, detoxifying toxins, and helps in the healing process. A transcription factor, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), contributes to a variety of physiological and pathological conditions, including immune response, cell death, cell survival, and inflammatory processes. During the pathogenesis of a burn wound, upregulation of various cytokines and growth factors lead to undesirable tissue inflammation. Thus, NF-κB, a dominant moderator of inflammation, needs to be altered to prove beneficial to the treatment of burns or other inflammation-associated diseases. This review addresses the relationship between NF-κB and elevated inflammation in a burn condition that could potentially be altered to induce an early wound-healing mechanism of burn wounds.

Indexed as

AnimalsBurnsHumansInflammationNF-kappa BReactive Oxygen SpeciesNF-kappa BReactive Oxygen SpeciesAntioxidantBurn injuryInflammation controlNF-κbWound healing

Identifiers

PMID33245371
OpenAlexW3109477632

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.