ArticleScientific reports2024
Causal relationship between lipidome and acute respiratory distress syndrome.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Therapeutic plasmapheresis in a young infant with severe hypertriglyceridemia: a case report.Clinical pediatric endocrinology : case reports and clinical investigations : official journal of the Japanese Society for Pediatric Endocrinology · 2026Article
- Mechanisms and therapeutics of immunometabolic reprogramming driving macrophage-ECs interactions in sepsis-associated ARDS from the gut-lung axis perspective.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
Acute respiratory distress syndrome (ARDS), with high morbidity and mortality, is a common clinical syndrome of acute respiratory failure caused by diffuse lung inflammation and edema. ARDS can precipitate in various ways. The complex pathophysiology of ARDS involves the activation and dysregulation of multiple metabolisms and immune responses. Using summary-level data from a genome-wide association study (GWAS), a two-sample Mendelian randomization (MR) analysis of 179 genetically predicted lipid species and ARDS (375 cases, 406,518 controls) was performed and validated in plasma and pulmonary edema fluid from 24 patients. Furthermore, we used a two-step MR to quantify the effect of immune cell-mediated lipids on ARDS. We identified 8 lipids (Cholesterol, Phosphatidylcholine (14:0_16:0), Phosphatidylcholine (16:0_20:5), Phosphatidylcholine (18:0_18:2), Phosphatidylethanolamine (18:1_18:1), Triacylglycerol (51:2), Triacylglycerol (52:4), and Triacylglycerol (54:3) ) associated with ARDS. The proportions of genetically-predicted lipids mediated by the four types of immune cells were determined. Sensitivity analysis did not reveal any obvious pleiotropy or heterogeneity. Our study demonstrates the power of multivariate genetic analysis in correlated lipidomic data and reveals genetic links between ARDS and lipid species beyond standard lipids.
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Registered trials
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