SynthesisFrontiers in immunology2025
Malondialdehyde-acetaldehyde modified macromolecules and resulting autoantibodies in rheumatoid arthritis pathogenesis: a Systematic Literature Review.
Synthesis in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Emerging Therapeutics in Rheumatoid Arthritis.Current rheumatology reports · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Objective: Substantial progress has been made in understanding the involvement of malondialdehyde-acetaldehyde (MAA) adducts in rheumatoid arthritis (RA) pathogenesis. This systematic review synthesizes current evidence on the role of MAA-modified macromolecules and anti-MAA antibodies in the development, manifestation, and progression of RA. Methods: MEDLINE, EMBASE, the Cochrane Library, Scopus, and SciFinder were searched through May 6, 2025. Studies were screened based on predefined inclusion/exclusion criteria. Study characteristics were extracted, and quality assessments were performed. Results: MAA-modified proteins and MAA-specific autoreactive B cells are elevated in synovial and lung tissues of RA patients. Anti-MAA antibodies are enriched in RA-derived synovial fluids compared to serum. Serum levels of anti-MAA IgG and IgA are increased prior to RA onset, and though not RA-specific, were higher in RA patients than those with other conditions. Anti-MAA antibodies do not cross-react with other autoantibodies, such as anti-citrullinated protein autoantibodies, and can be detected in sera from seronegative RA patients. Elevated anti-MAA antibody levels correlate with progression of joint, lung, and cardiovascular complications, as well as biologic treatment responses. Human and animal studies have begun to elucidate mechanisms by which MAA and anti-MAA antibody might contribute to inflammatory and fibrotic changes in RA. Conclusions: This review provides a comprehensive overview of MAA and its involvement in RA pathogenesis. MAA adducts contribute to loss of immune tolerance and promote both inflammation and fibrosis in RA. Given associations of anti-MAA antibodies with RA disease activity and complications, MAA-related pathways hold promise as both biomarkers and treatment targets in RA. Systematic Review Registration: https://www.crd.york.ac.uk/PROSPERO/, identifier CRD4202454490.
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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.