ReviewCentral-European journal of immunology2020
Systemic lupus erythematosus and glycation process.
Review in Central-European journal of immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Elevated levels of advanced glycation end-products AGE10 in patients with reactive arthritis caused by Chlamydia trachomatis and Epstein-Barr virus infection.Immunologic research · 2026Article
- Article
- The RAGE Axis: A Relevant Inflammatory Hub in Human Diseases.Biomolecules · 2024Review
- Advanced glycation end product signaling and metabolic complications: Dietary approach.World journal of diabetes · 2023Review
- Glycation end-products specific auto-antibodies in Systemic Lupus Erythematosus.Bioinformation · 2022Article
- Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis.Journal of personalized medicine · 2021Article
- The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases.Molecules (Basel, Switzerland) · 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a disease of unclear causes, which leads to major immunological disorders. It is characterized by an abnormal immune system activity resulting in the production of autoantibodies. In patients, antibodies targeting normal nuclear components, double-stranded DNA (dsDNA), and phospholipids (cardiolipin) can be detected. The inflammatory process occurs in various tissues and organs, damaging their functions and structure. Disease's course includes stages of acute symptoms and remissions, and there is no known cure. Pathogenesis and biochemical pathways accompanying systemic lupus erythematosus are widely studied, as existing medication can only bring temporary relief to patients. The recent findings suggest that occurrence of SLE depends on interactions between genetic background of the disease and environmental risk factors such as exposure to tobacco smoke, chemical factors, and hormonal therapy. In the addition, chronic inflammation accompanying SLE disturbs oxidative/antioxidative balance. These processes are linked to intensified advanced glycation end products (AGEs) formation, thus level of AGEs themselves and their receptors (RAGE, sRAGE) are gaining researches attention.
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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.