ReviewExperimental gerontology2018
DNA damage, metabolism and aging in pro-inflammatory T cells: Rheumatoid arthritis as a model system.
Review in Experimental gerontology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed.
- Rheumatoid arthritis T cell and muscle oxidative metabolism associate with exercise-induced changes in cardiorespiratory fitness.Scientific reports · 2022Trial
- Decreased Peripheral Naïve T Cell Number and Its Role in Predicting Cardiovascular and Infection Events in Hemodialysis Patients.Frontiers in immunology · 2021Trial
- Lipid droplet-induced T cell death sustains autoimmune tissue inflammation.Cell metabolism · 2026Article
- The Linkage Between Ecotoxins Within Maximum Permissible Concentrations, Oxidative Stress and Antibodies Against Cyclic Citrullinated Peptides in Patients and Persons at Preclinic Stages of Rheumatoid Arthritis.International journal of molecular sciences · 2026Article
- High glucose-induced mitophagy accelerates premature aging of T cells in patients with rheumatoid arthritis.Clinical rheumatology · 2026Article
- RA-risk synovium exhibits DNA damage coupled with impaired DNA repair in fibroblasts.RMD open · 2026Article
- Immune Aging in Rheumatoid Arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2025Review
- Diverging effects of tumor necrosis factor inhibitors and conventional synthetic disease-modifying antirheumatic drugs on immunosenescence and inflammageing in rheumatoid arthritis: a cross-sectional analysis.Immunity & ageing : I & A · 2025Article
- To cleave or not and how? The DNA exonucleases and endonucleases in immunity.Genes & diseases · 2025Review
- Metabolic checkpoints in rheumatoid arthritis.Seminars in arthritis and rheumatism · 2025Review
- An in-depth understanding of the role and mechanisms of T cells in immune organ aging and age-related diseases.Science China. Life sciences · 2025Review
- The small molecule inhibitor 3PO is a modulator of neutrophil metabolism, ROS production, and NET release.Clinical and experimental immunology · 2025Article
- Biomaterials for Modulating the Immune Microenvironment in Rheumatoid Arthritis.BME frontiers · 2025Review
- Recent Advances in Biomimetic Drug Delivery for Rheumatoid Arthritis Treatment.International journal of nanomedicine · 2025Review
- Modulating the gut-immune axis to alleviate rheumatoid arthritis: mechanistic insights and therapeutic potential of traditional Chinese medicine.Frontiers in immunology · 2025Review
- The relationship between non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) and rheumatoid arthritis: a cross-sectional study.Frontiers in nutrition · 2025Article
- Iron and energy metabolic interactions in Treg-mediated immune regulation.Frontiers in immunology · 2025Review
- Benefit delayed immunosenescence by regulating CD4Aging cell · 2024Review
- Are immunosenescent T cells really senescent?Aging cell · 2024Review
- Nature of the Association between Rheumatoid Arthritis and Cervical Cancer and Its Potential Therapeutic Implications.Nutrients · 2024Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The aging process is the major driver of morbidity and mortality, steeply increasing the risk to succumb to cancer, cardiovascular disease, infection and neurodegeneration. Inflammation is a common denominator in age-related pathologies, identifying the immune system as a gatekeeper in aging overall. Among immune cells, T cells are long-lived and exposed to intense replication pressure, making them sensitive to aging-related abnormalities. In successful T cell aging, numbers of naïve cells, repertoire diversity and activation thresholds are preserved as long as possible; in maladaptive T cell aging, protective T cell functions decline and pro-inflammatory effector cells are enriched. Here, we review in the model system of rheumatoid arthritis (RA) how maladaptive T cell aging renders the host susceptible to chronic, tissue-damaging inflammation. In T cells from RA patients, known to be about 20years pre-aged, three interconnected functional domains are altered: DNA damage repair, metabolic activity generating energy and biosynthetic precursor molecules, and shaping of plasma membranes to promote T cell motility. In each of these domains, key molecules and pathways have now been identified, including the glycolytic enzymes PFKFB3 and G6PD; the DNA repair molecules ATM, DNA-PKcs and MRE11A; and the podosome marker protein TKS5. Some of these molecules may help in defining targetable pathways to slow the T cell aging process.
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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.