ArticleArthritis & rheumatology (Hoboken, N.J.)2015
Malondialdehyde-acetaldehyde adducts and anti-malondialdehyde-acetaldehyde antibodies in rheumatoid arthritis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 3 of them syntheses that pooled it.
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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.
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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.
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Who cites it
93 citing papers in PubMed, 3 syntheses or guidelines pooled it, 150 citations in OpenAlex.
- Malondialdehyde-acetaldehyde modified macromolecules and resulting autoantibodies in rheumatoid arthritis pathogenesis: a Systematic Literature Review.Frontiers in immunology · 2025Pooled it
- Assessment of anti-malondialdehyde-acetaldehyde antibody frequencies in rheumatoid arthritis with new data from two independent cohorts, meta-analysis, and meta-regression.Arthritis research & therapy · 2023Pooled it
- Oxidative Stress Relevance in the Pathogenesis of the Rheumatoid Arthritis: A Systematic Review.BioMed research international · 2016Pooled it
- Attenuation of Cardiac Dysfunction in the Collagen-Induced Arthritis Mouse Model Mediated by a Reactive Aldehyde Species Inhibitor.International journal of molecular sciences · 2026Article
- Complement Activation by Post-Translationally Modified Proteins: Links to Chronic Inflammation and Autoimmunity.Immunological reviews · 2026Review
- Impact of Dual Rheumatoid Factor and Anticitrullinated Protein Antibody Seropositive, Single Seropositive, and Seronegative Rheumatoid Arthritis on Outcomes.Arthritis care & research · 2026Article
- Anti-Modified Protein Antibodies in Rheumatoid Arthritis: Pathogenic, Protective, or Passive Bystander?Immunological reviews · 2026Review
- 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
- The redox-sensitive protein HMGB1: intracellular and extracellular roles.Experimental & molecular medicine · 2026Review
- Biomarkers in Rheumatoid Arthritis: From Traditional Serology to Precision Medicine Integration.Diagnostics (Basel, Switzerland) · 2026Review
- Body mass index as a key determinant of oxidative stress in women undergoing infertility treatment.Frontiers in reproductive health · 2026Article
- Review
- Rheumatoid Arthritis: A Comprehensive Review of Etiology, Pathophysiology, and Innovative Therapeutic Advancements.Current pharmaceutical design · 2026Review
- Molecular basis of post-translational neoantigen generation in rheumatoid arthritis: breaking immunological tolerance and implications for targeted therapy.Frontiers in immunology · 2026Review
- Citrullinated and Malondialdehyde-Acetaldehyde-Modified Fibrinogen Activates Macrophages and Promotes Coronary Endothelial Cell Inflammation.Current issues in molecular biology · 2025Article
- Oral Microbiota Linking Humoral Response, Periodontitis and Atherosclerosis.Journal of clinical periodontology · 2025Article
- Autoantibodies as prognostic markers in rheumatoid arthritis.Journal of translational autoimmunity · 2025Review
- Protective effects of Catalpol to attenuate TNF- α and collagen-induced inflammation in vitro HFLS-RA cells and in vivo mice models for the treatment of rheumatoid arthritis.Clinical rheumatology · 2025Article
- The Veterans Affairs Rheumatoid Arthritis Registry: A unique population in rheumatoid arthritis research.Seminars in arthritis and rheumatism · 2025Review
- Citrullinated and malondialdehyde-acetaldehyde-modified fibrinogen activates macrophages and promotes profibrotic responses in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2025Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
objectiveMalondialdehyde-acetaldehyde (MAA) adducts are a product of oxidative stress associated with tolerance loss in several disease states. This study was undertaken to investigate the presence of MAA adducts and circulating anti-MAA antibodies in patients with rheumatoid arthritis (RA).
methodsSynovial tissue from patients with RA and patients with osteoarthritis (OA) were examined for the presence of MAA-modified and citrullinated proteins. Anti-MAA antibody isotypes were measured in RA patients (n = 1,720) and healthy controls (n = 80) by enzyme-linked immunosorbent assay. Antigen-specific anti-citrullinated protein antibodies (ACPAs) were measured in RA patients using a multiplex antigen array. Anti-MAA isotype concentrations were compared in a subset of RA patients (n = 80) and matched healthy controls (n = 80). Associations of anti-MAA antibody isotypes with disease characteristics, including ACPA positivity, were examined in all RA patients.
resultsExpression of MAA adducts was increased in RA synovial tissue compared to OA synovial tissue, and colocalization with citrullinated proteins was found. Increased levels of anti-MAA antibody isotypes were observed in RA patients compared to controls (P < 0.001). Among RA patients, anti-MAA antibody isotypes were associated with seropositivity for ACPAs and rheumatoid factor (P < 0.001) in addition to select measures of disease activity. Higher anti-MAA antibody concentrations were associated with a greater number of positive antigen-specific ACPA analytes (expressed at high titer) (P < 0.001) and a higher ACPA score (P < 0.001), independent of other covariates.
conclusionMAA adduct formation is increased in RA and appears to result in robust antibody responses that are strongly associated with ACPAs. These results support speculation that MAA formation may be a cofactor that drives tolerance loss, resulting in the autoimmune responses characteristic of RA.
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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.