ArticleArthritis & rheumatology (Hoboken, N.J.)2023
Platelet LGALS3BP as a Mediator of Myeloid Inflammation in Systemic Lupus Erythematosus.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- Nutritional status-dependent DNA methylation modifications on adipose tissue in systemic lupus erythematosus women following folic acid and vitamin B12 supplementation: a randomized double-blind placebo-controlled trial.Clinical epigenetics · 2026Trial
- Article
- A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.Annals of the rheumatic diseases · 2026Article
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Secretory LGALS3BP exacerbates sepsis-associated liver dysfunction by activating inflammasome-mediated pyroptosis.Cell death discovery · 2026Article
- TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- A platelet transcriptomic signature of thromboinflammation predicts cardiovascular risk.JCI insight · 2025Article
- Bone marrow B lymphopoiesis accelerates early cerebral amyloid pathology.Signal transduction and targeted therapy · 2025Article
- Elucidating the role of LGALS3BP in coronary atherosclerosis: integrating bioinformatics and machine learning for advanced insights.Journal of cardiothoracic surgery · 2025Article
- Platelets as drivers of immunothrombosis in rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Pathogenic strains of a gut commensal drive systemic platelet activation and thromboinflammation in lupus nephritis.bioRxiv : the preprint server for biology · 2025Article
- Investigating Overlapping Genetic Factors and Novel Causal Genes in Autoimmune Diseases: A Transcriptome-Wide Association and Multiomics Study.International journal of genomics · 2025Article
- Scavenger receptors: key players in the immunological puzzle of lupus.Frontiers in lupus · 2025Article
- Molecular intersections of traumatic brain injury and Alzheimer's disease: the role of ADMSC-derived exosomes and hub genes in microglial polarization.Metabolic brain disease · 2024Article
- Platelet activation through CD62P and the formation of platelet-monocyte complexes are associated with the exacerbation of mucosal inflammation in patients with ulcerative colitis.Scientific reports · 2024Article
- Biomarkers for systemic lupus erythematosus: A scoping review.Immunity, inflammation and disease · 2024Article
- Inhibiting the P2YJACC. Basic to translational science · 2024Article
- A Platelet Reactivity ExpreSsion Score derived from patients with peripheral artery disease predicts cardiovascular risk.Nature communications · 2024Observational
- Alternative platelet differentiation pathways initiated by nonhierarchically related hematopoietic stem cells.Nature immunology · 2024Article
- Impaired bisecting GlcNAc reprogrammed M1 polarization of macrophage.Cell communication and signaling : CCS · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
objectivePlatelets are mediators of inflammation with immune effector cell properties and have been implicated in the pathogenesis of systemic lupus erythematosus (SLE). This study investigated the role of platelet-associated lectin, galactoside-binding, soluble 3 binding protein (LGALS3BP) as a mediator of inflammation in SLE and as a potential biomarker associated with clinical phenotypes.
methodsWe performed RNA sequencing on platelets from patients with SLE (n = 54) and on platelets from age-, sex-, and race/ethnicity-matched healthy controls (n = 18) and measured LGALS3BP levels in platelet releasate and in circulating serum. We investigated the association between LGALS3BP levels and the prevalence, disease severity, and clinical phenotypes of SLE and studied platelet-mediated effects on myeloid inflammation.
resultsPlatelets from patients with SLE exhibited increased expression of LGALS3BP (fold change 4.0, adjusted P = 6.02 × 10
conclusionsOur results support that platelets act as potent effector cells that contribute to the pathogenesis of SLE by secreting proinflammatory LGALS3BP, which also represents a novel biomarker of SLE clinical activity.
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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.