ArticleHeliyon2023
Critical role of lectin pathway mediated by MBL-associated serine proteases in complement activation for the pathogenesis in systemic lupus erythematosus.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Advances in the lectin pathway in systemic lupus erythematosus: from clinical correlations and mechanisms to targeted interventions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Lectin pathway components and autoantibodies as novel immunological biomarkers in systemic lupus erythematosus (SLE) patients from Western India.Scientific reports · 2025Article
- Differential Expression of ARG1 and MRC2 in Retinal Müller Glial Cells During Autoimmune Uveitis.Biomolecules · 2025Article
- Complement Activation in Nephrotic Glomerular Diseases.Biomedicines · 2024Review
- Extracellular Vesicles in the Pathogenesis, Clinical Characterization, and Management of Dermatomyositis: A Narrative Review.International journal of molecular sciences · 2024Review
- The Lectin Pathway of the Complement System-Activation, Regulation, Disease Connections and Interplay with Other (Proteolytic) Systems.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In complement activation system, although the classical pathway has shown to play a critical role for the pathogenesis of SLE, the role of lectin pathway has remained unknown in the pathogenesis of SLE. As Mannose-binding lectin-associated serine proteases (MASPs) are associated with activation of the lectin pathway, we conducted this study to clarify MASPs associations in the pathogenesis of SLE. We evaluated the serum level of MASPs (MASP-1 and MASP-2) in total 68 SLE patients consisting of 15 patients with biopsy-confirmed membranous lupus nephritis (M-LN), 35 patients with biopsy-confirmed proliferative lupus nephritis (P-LN), and 18 SLE patients without LN (non-LN). Our data showed that the serum levels of MASPs were reduced in both P-LN and non-LN although those of M-LN were not reduced. Our data show that the lectin pathway mediated by MASPs plays a critical role for the pathogenesis of SLE except for M-LN.
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Registered trials
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