Evidence map›Paper›PMID 29088923›Full record

ReviewAntioxidants & redox signaling2018

Oxidative Modifications in Tissue Pathology and Autoimmune Disease.

Mei-Ling Yang, Hester A Doyle, Steven G Clarke, Kevan C Herold, Mark J Mamula

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  16. Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022
    Review
  17. Article
  18. 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

5 authors at 2 institutions in 1 country.

Mei-Ling Yang1 Section of Rheumatology, Yale University School of Medicine , New Haven, Connecticut.
Hester A Doyle1 Section of Rheumatology, Yale University School of Medicine , New Haven, Connecticut.
Steven G Clarke3 Department of Chemistry and Biochemistry, University of California , Los Angeles, Los Angeles, California.
Kevan C Herold2 Department of Internal Medicine, Yale University School of Medicine , New Haven, Connecticut.
Mark J Mamula1 Section of Rheumatology, Yale University School of Medicine , New Haven, Connecticut.
Yale University · USUniversity of California, Los Angeles · US

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Kevan C Herold, GERALD I SHULMAN · 1993 to 2026
$44.0M
Epigenetic, Protein, and Cellular Biomarkers of Beta Cell Function in T1DUC4DK104205 · NIDDK · YALE UNIVERSITY · PI HEROLD, KEVAN C · 2014 to 2014
$2.5M
NIDDK NIH HHS P30 DK045735NIDDK NIH HHS UC4 DK104205
6 · The paper itself

Abstract

significanceVarious autoimmune syndromes are characterized by abnormalities found at the level of tissues and cells, as well as by microenvironmental influences, such as reactive oxygen species (ROS), that alter intracellular metabolism and protein expression. Moreover, the convergence of genetic, epigenetic, and even environmental influences can result in B and T lymphocyte autoimmunity and tissue pathology. Recent Advances: This review describes how oxidative stress to cells and tissues may alter post-translational protein modifications, both directly and indirectly, as well as potentially lead to aberrant gene expression. For example, it has been clearly observed in many systems how oxidative stress directly amplifies carbonyl protein modifications. However, ROS also lead to a number of nonenzymatic spontaneous modifications including deamidation and isoaspartate modification as well as to enzyme-mediated citrullination of self-proteins. ROS have direct effects on DNA methylation, leading to influences in gene expression, chromosome inactivation, and the silencing of genetic elements. Finally, ROS can alter many other cellular pathways, including the initiation of apoptosis and NETosis, triggering the release of modified intracellular autoantigens. CRITICAL ISSUES: This review will detail specific post-translational protein modifications, the pathways that control autoimmunity to modified self-proteins, and how products of ROS may be important biomarkers of tissue pathogenesis. FUTURE DIRECTIONS: A clear understanding of the many pathways affected by ROS will lead to potential therapeutic manipulations to alter the onset and/or progression of autoimmune disease.

Indexed as

AnimalsAutoimmune DiseasesDNA MethylationHumansOxidation-ReductionProtein CarbonylationProtein Processing, Post-TranslationalProteinsReactive Oxygen SpeciesProteinsReactive Oxygen Speciesautoantigensautoimmunitycarbonylationcitrullinationpost-translational modificationtype 1 diabetes

Identifiers

PMID29088923
PMCPMC6166690
OpenAlexW2766831773

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.