Evidence map›Paper›PMID 35432339›Full record

ArticleFrontiers in immunology2022

Chronically Elevated

Lara K Abramowitz, John A Hanover

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Frontiers in immunology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. 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 at 2 institutions in 1 country.

Lara K AbramowitzLaboratory of Cell and Molecular Biology, National Institute for Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States.
John A HanoverLaboratory of Cell and Molecular Biology, National Institute for Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States.
National Institute of Diabetes and Digestive and Kidney Diseases · USNational Institutes of Health · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Enzymes of O-GlcNAc cycling linked to type-2 diabetes and neurodegenerationZIADK060103 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$20.8M
Calmodulin-driven Nuclear Trafficking linked to diabetes and insulin signalingZIADK060102 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$8.5M
6 · The paper itself

Abstract

Inflammation is the immune response to harmful stimuli, including pathogens, damaged cells and toxic compounds. However, uncontrolled inflammation can be detrimental and contribute to numerous chronic inflammatory diseases, such as insulin resistance. At the forefront of this response are macrophages, which sense the local microenvironment to respond with a pro-inflammatory, M1-polarized phenotype, or anti-inflammatory, M2-polarized phenotype. M1 macrophages upregulate factors like pro-inflammatory cytokines, to promote inflammatory signaling, and inducible Nitric Oxide Synthase (iNOS), to produce nitric oxide (NO). The generated NO can kill microorganisms to protect the body, but also signal back to the macrophage to limit pro-inflammatory cytokine production to maintain macrophage homeostasis. Thus, the tight regulation of iNOS in macrophages is critical for the immune system. Here, we investigated how elevation of the nutrient-sensitive posttranslational modification,

Indexed as

CytokinesNitric OxideAcetylglucosaminidaseHumansInflammationInterleukin-6MacrophagesAcetylglucosaminidaseCytokinesInterleukin-6Nitric OxidecytokinesinflammationiNOSmacrophagesO-GlcNAcaseO-GlcNAcylation

Identifiers

PMID35432339
PMCPMC9010940
OpenAlexW4220735424

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.