ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2018
Inflammation, a significant player of Ataxia-Telangiectasia pathogenesis?
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 45 citations in OpenAlex.
- cGAS-STING axis: A central regulator of neural homeostasis and neuroinflammatory pathogenesis.Neural regeneration research · 2026Article
- ATM counteracts chromatin-bound cGAS during DNA replication.Nature cell biology · 2026Article
- Novel genetic variants identification and immune profiling in ataxia telangiectasia patients.Journal of translational medicine · 2026Article
- Clinical challenges following early detection of ataxia telangiectasia through SCID newborn screening.Journal of human immunity · 2025Review
- Hematopoietic stem cell metabolism within the bone marrow niche - insights and opportunities.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- ATM Expression and Activation in Ataxia Telangiectasia Patients with and without Class Switch Recombination Defects.Journal of clinical immunology · 2025Article
- A-T neurodegeneration and DNA damage-induced transcriptional stress.DNA repair · 2024Review
- The Role of cGAS-STING in Age-Related Diseases from Mechanisms to Therapies.Aging and disease · 2023Review
- DNA damage and repair in age-related inflammation.Nature reviews. Immunology · 2023Review
- NRF2 Mediates Cellular Resistance to Transformation, Radiation, and Inflammation in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Targeting the DNA repair enzymes MTH1 and OGG1 as a novel approach to treat inflammatory diseases.Basic & clinical pharmacology & toxicology · 2022Review
- Progressive Depletion of B and T Lymphocytes in Patients with Ataxia Telangiectasia: Results of the Italian Primary Immunodeficiency Network.Journal of clinical immunology · 2022Article
- Review
- Deficiency of ataxia-telangiectasia mutated kinase modulates functional and biochemical parameters of the heart in response to Western-type diet.American journal of physiology. Heart and circulatory physiology · 2021Article
- Hallmarks of Cancers: Primary Antibody DeficiencyFrontiers in immunology · 2021Review
- Vasculogenic Mimicry Formation Predicts Tumor Progression in Oligodendroglioma.Pathology oncology research : POR · 2021Article
- Nucleic Acid Immunity and DNA Damage Response: New Friends and Old Foes.Frontiers in immunology · 2021Review
- Update on DNA-Double Strand Break Repair Defects in Combined Primary Immunodeficiency.Current allergy and asthma reports · 2020Review
- Review
- Mitochondria at the crossroads of ATM-mediated stress signaling and regulation of reactive oxygen species.Redox biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAtaxia-Telangiectasia (A-T) syndrome is an autosomal recessive neurodegenerative disorder characterized by cerebellar ataxia, oculocutaneous telangiectasia, immunodeficiency, chromosome instability, radiosensitivity, and predisposition to malignancy. There is growing evidence that A-T patients suffer from pathologic inflammation that is responsible for many symptoms of this syndrome, including neurodegeneration, autoimmunity, cardiovascular disease, accelerated aging, and insulin resistance. In addition, epidemiological studies have shown A-T heterozygotes, somewhat like deficient patients, are susceptible to ionizing irradiation and have a higher risk of cancers and metabolic disorders. AREA COVERED: This review summarizes clinical and molecular findings of inflammation in A-T syndrome.
conclusionAtaxia-Telangiectasia Mutated (ATM), a master regulator of the DNA damage response is the protein known to be associated with A-T and has a complex nuclear and cytoplasmic role. Loss of ATM function may induce immune deregulation and systemic inflammation.
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.