ArticleRheumatology (Oxford, England)2024
Kidney whole-transcriptome profiling in primary antiphospholipid syndrome reveals complement, interferons and NETs-related gene expression.
Article in Rheumatology (Oxford, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Molecular Stratification of Antiphospholipid Syndrome Through Integrative Analysis of the Whole-Blood RNA Transcriptome.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- RNA sequencing-derived gene co-expression and drug-gene interaction analysis reveal STAT1 as a potential therapeutic target in thrombotic antiphospholipid syndrome.Frontiers in immunology · 2026Article
- Antiphospholipid Syndrome and the Kidney.Kidney international reports · 2025Review
- Platelets as drivers of immunothrombosis in rheumatic diseases.Nature reviews. Rheumatology · 2025Review
- Perspective on Renal Involvement in Antiphospholipid Syndrome: Implications for Diagnosis, Pathogenesis, and Treatment.Journal of clinical medicine · 2025Review
- Novel advances on pathophysiological mechanisms, clinical manifestations, and treatment of antiphospholipid syndrome.Frontiers in immunology · 2025Review
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Authors and funding
7 authors.
Funding
Abstract
objectivePathogenesis of antiphospholipid syndrome (APS) remains poorly elucidated. We aimed to evaluate for the first time kidney transcriptome profiles in primary APS vs systemic lupus erythematosus (SLE) and control subjects.
methodsWe performed RNA sequencing on archival formalin-fixed paraffin-embedded kidney biopsies from APS (n = 4), SLE (n = 5) and control (n = 3) individuals, differential gene expression analysis (DGEA) and enrichment analysis using gene ontology (GO) and CORUM, KEGG and Reactome pathway databases.
resultsTwo-dimensional projection showed a distinct gene profile in primary APS vs control kidneys samples, but similar to SLE. DGEA in APS vs controls returned 276 upregulated and 217 downregulated genes, while the comparison between APS and SLE identified 75 upregulated and 111 downregulated genes. In 276 upregulated genes, enriched GO terms were (innate) immune response, inflammatory response, leucocyte and lymphocyte activation, cytokine production and T cell activation. CORUM and KEGG revealed complement-related genes (C3, C4A, C4B). Expression levels showed logFC values of 2.25 (P = 1.58e-05) for C3, 2.17 (P = 2.69e-06) for C4A and 2.135 (P = 3.7e-06) for C4B in APS vs controls, without differences between APS and SLE. Interferon (IFN) alpha/beta signalling was revealed by Reactome. Expression levels of nine IFN-regulated genes found upregulated in APS vs control kidneys (P-values ≤ 0.001 for all). Examining neutrophil-extracellular traps (NETs)-related gene expression, 13 of 15 upregulated NETs-related genes exhibited higher expression in APS vs controls but not vs SLE.
conclusionComplement, interferon and NETs-related genes are highly expressed in APS kidney tissues, similarly to SLE, pointing out the role of innate immunity in APS nephropathy pathogenesis and potential treatment targets.
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