ArticleJournal of hepato-biliary-pancreatic sciences2026
Integrative Genomics Reveals Causal Pleiotropy and Therapeutic Opportunities at the Interface of Acute Pancreatitis and Infection.
Article in Journal of hepato-biliary-pancreatic sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Factors associated with sarcopenia in elderly patients with type 2 diabetes mellitus.Frontiers in endocrinology · 2026Pooled it
- Integrated post-GWAS, single-cell, and functional analyses prioritizeFrontiers in immunology · 2026Article
- Association between the ratio of uric acid to high-density lipoprotein cholesterol (UHR) and the abnormal risk of sarcopenia: Evidence from two large population-based surveys and interpretable machine learning-driven sarcopenia screening.Therapeutic advances in endocrinology and metabolism · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUnderstanding the genetic links between acute pancreatitis (AP) and its infectious comorbidities is crucial for prognosis and therapy, yet remains underexplored.
methodsWe conducted a comprehensive post-GWAS analysis using large-scale summary statistics for AP and 16 infectious diseases. To pinpoint pleiotropic genes, we integrated multi-omics data via transcriptome-wide and proteome-wide association studies, and resolved cell-type-specific effects using single-cell analysis. Extensive locus colocalization analyses were performed to validate our findings by estimating the probability of shared causal variants.
resultsThis computational discovery phase prioritized 29 high-confidence pleiotropic genes, including established loci (SPINK1, CRP) and novel candidates (ERBB2, ALDH2, FLOT1). To functionally validate and contextualize these findings, we performed bulk transcriptomic analysis on peripheral blood from AP patients and employed gsMap, a spatial GWAS mapping algorithm, to integrate our genetic data with transcriptomics from a murine AP model, comparing pathological versus normal tissue. These analyses confirmed that the identified genes are dynamically regulated in a severity-dependent manner in patients and are activated within specific pathological niches in pancreatic tissue.
conclusionIn conclusion, this study provides a genetic map linking AP and its infectious comorbidities, offering insights into potential prevention strategies and highlighting novel therapeutic targets for further investigation and validation.
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