ArticleClinics (Sao Paulo, Brazil)2026
Identifying prioritization of potential targets for idiopathic pulmonary fibrosis: Proteome-wide Mendelian randomization and colocalization analyses.
Article in Clinics (Sao Paulo, Brazil), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundIdiopathic Pulmonary Fibrosis (IPF) is a chronic and progressive lung disorder characterized by limited therapeutic options. Thus, identifying new therapeutic targets for IPF is imperative.
methodsThe authors employed 2 large-scale circulating proteomic and IPF GWAS (Ncase = 2189, Ncontrol = 407,609) to conduct proteome-wide Mendelian randomization meta-analysis. Subsequently, the authors utilized Summary Mendelian Randomization analysis and Bayesian colocalization to enhance the screening of proteins. Lastly, MR analysis of protein-protein level ratio, two-step MR method, enrichment analysis, Protein-Protein Interaction (PPI), and druggability assessment were applied to explore the potential mechanisms of candidate proteins.
resultsThrough proteome-wide Mendelian randomization analysis and multiple validations, the authors identified 3 plasma proteins significantly associated with IPF. With strong evidence of colocalization and consistent support from SMR analysis, the gene-predicted MASP1 was correlated with decreased IPF risk (OR
conclusionsOur proteome-wide Mendelian Randomization analysis highlighted MASP1, S100A11, and WFIKKN2 as potential targets for further clinical investigation in IPF. The specific mechanisms by which these proteins influence IPF pathogenesis require further elucidation through continued research.
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