ReviewRheumatology international2022
The relationship between defects in DNA repair genes and autoinflammatory diseases.
Review in Rheumatology international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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.
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.
Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Ultrarare Variants in DNA Damage Repair and Mitochondrial Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome and Acute Behavioral Regression in Neurodevelopmental Disorders.Developmental neuroscience · 2026Article
- Transcriptomic Analysis Reveals the Growth Regulatory Mechanisms in Diploid, Triploid, and Tetraploid Pacific Oyster (Animals : an open access journal from MDPI · 2025Article
- Ultrarare Variants in DNA Damage Repair Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome or Acute Behavioral Regression in Neurodevelopmental Disorders.Developmental neuroscience · 2025Article
- Exploration of effective biomarkers for venous thrombosis embolism in Behçet's disease based on comprehensive bioinformatics analysis.Scientific reports · 2024Article
- JAK inhibitors improve ATP production and mitochondrial function in rheumatoid arthritis: a pilot study.Rheumatology international · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue inflammation and damage with the abnormal and overactivation of innate immune system results with the development of a hereditary disease group of autoinflammatory diseases. Multiple numbers of DNA damage develop with the continuous exposure to endogenous and exogenous genotoxic effects, and these damages are repaired through the DNA damage response governed by the genes involved in the DNA repair mechanisms, and proteins of these genes. Studies showed that DNA damage might trigger the innate immune response through nuclear DNA accumulation in the cytoplasm, and through chronic DNA damage response which signals itself and/or by micronucleus. The aim of the present review is to identify the effect of mutation that occurred in DNA repair genes on development of DNA damage response and autoinflammatory diseases.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.