ArticleCell reports. Medicine2025
RSAD2: A pathogenic interferon-stimulated gene at the maternal-fetal interface of patients with systemic lupus erythematosus.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Macrophage RSAD2 Couples mtDNA Synthesis With a Self-Amplifying Inflammatory Circuit to Orchestrate Tissue Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RSAD2/VIPERIN and CMPK2 coordinate an immunometabolic response to Epstein-Barr Virus.PLoS pathogens · 2026Article
- Spatially resolved fetal and maternal cell contributions to severe preeclampsia across gestation.Science advances · 2026Article
- A dual-pronged host-directed therapeutic targeting cyclophilin A and pathogenic interferon response abrogates virus-triggered pregnancy pathologies.Nature communications · 2026Article
- Comparison of BAFF and type I IFN activity in blood and placenta in SLE and healthy pregnancies.Lupus science & medicine · 2026Article
- Fertility, pregnancy and lactation in women with systemic lupus erythematosus.Nature reviews. Rheumatology · 2026Review
- T-bet Fate Mapping Reveals Gestational Stage-Specific Transcriptional Adaptation of Decidual NK Cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Upregulated ZBP1 Is Associated with B-Cell Dysregulation in Systemic Lupus Erythematosus.Biomedicines · 2026Article
- RSAD2/VIPERIN and CMPK2 Coordinate an Immunometabolic Response to Epstein-Barr Virus.bioRxiv : the preprint server for biology · 2026Article
- Beyond Viral Restriction: The Metabolic Dimensions of Interferon-Stimulated Genes in Antiviral Immunity.Viruses · 2026Review
- Immunopathogenesis of accelerated atherosclerosis in systemic lupus erythematosus: from innate and adaptive dysregulation to clinical implications.Frontiers in immunology · 2026Review
- Effect of Maternal Administration with All-Trans Retinoic Acid on Lungs of Neonatal Pigs.Veterinary sciences · 2025Article
- Interferon-stimulated Viperin impairs Treg function in autoimmune thrombocytopenia.Cell communication and signaling : CCS · 2025Article
- Efficient integration of spatial omics data for joint domain detection, matching, and alignment with stMSA.Genome research · 2025Article
- Viperin: A Multifunctional Protein in Antiviral Immunity and Disease Pathogenesis.Pathogens (Basel, Switzerland) · 2025Review
- Immunohistochemical analysis reveals higher Myxovirus resistance protein 1 expression and increased macrophage count in placentas from patients with systemic rheumatic diseases.Rheumatology international · 2025Article
- Targeting pathogenic interferon-stimulated gene RSAD2 improves pregnancy outcomes in systemic lupus erythematosus models.Cell reports. Medicine · 2025Article
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pregnancy disorders in patients with autoimmune diseases or viral infections are often associated with an excessive response of type I interferons. We identify radical S-adenosyl methionine domain containing 2 (RSAD2) as a pathogenic interferon-stimulated gene (ISG) associated with pregnancy complications in systemic lupus erythematosus (SLE). The increased expression of RSAD2 mainly occurs in macrophages and structural cell populations at the maternal-fetal interface of pregnant patients with SLE. The elevation of RSAD2 leads to the accumulation of diacylglycerol lipids in the placenta, impairing the necessary vascular development for the fetus. Depletion of Rsad2 in pregnant mice models exposed to type I interferon inducers significantly reduces lipid accumulation, vascular injury, and embryo development disorders. An RSAD2 inhibitor, L-chicoric acid (LCA), alleviates lipid accumulation and vascular damage, improving pregnancy outcomes in SLE-induced and spontaneous mouse models. This study proposes the potential of targeting RSAD2 to improve pregnancy outcomes in individuals with heightened type I interferon response.
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