Exploring the Causal Relationship Between Plasma Proteins and Systemic Lupus Erythematosus: A Mendelian Randomization Study

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Background: Systemic lupus erythematosus (SLE) is a complex autoimmune disease that severely impacts patient quality of life. Current treatments primarily manage symptoms rather than cure the disease, emphasizing the need for a deeper understanding of its pathogenesis and the discovery of novel therapeutic targets. Circulating proteins are thought to play a critical role in SLE risk, but their causal relationships remain underexplored.Methods: This study used pQTL and genome-wide association study (GWAS) data to perform a two-sample Mendelian randomization (MR) analysis to investigate the genetic causal relationships between circulating proteins and SLE. We identified proteins potentially associated with SLE risk and further analyzed their roles in immune regulation and inflammation using Protein-Protein Interaction (PPI) networks. Colocalization analysis was conducted to validate the associations of key proteins with SLE.Results: Our analysis identified 82 plasma proteins potentially causally linked to SLE risk (p < 0.05). Colocalization analysis confirmed the association of proteins such as TNFAIP3, PDHX, and CTSF with SLE, underscoring their critical role in disease pathogenesis. Additionally, PPI network analysis revealed that these proteins are involved in immune modulation and inflammatory pathways, further supporting their relevance as therapeutic targets.Conclusion: This study identifies 82 plasma proteins that may play a causal role in SLE, with TNFAIP3, PDHX, and CTSF emerging as promising therapeutic targets. These findings provide a foundation for future research aimed at developing precision therapies for SLE.

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