American journal of hypertension · 2026
Role of Transitional %B Cells in Mediating the Effect of Phosphatidylinositol (16:0_18:1) on Aortic Dissection.
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Ma Likang, Tang Lele, Jin Lei, Li Jiakang, Li Haoyu, Chen Liangwan, Qiu Zhihuang
Аннотация
BACKGROUND: This study investigates the causal associations between specific plasma lipids, immune cells, and aortic dissection (AD) pathogenesis, and explores immune cells as mediators in this relationship.
METHODS: This study used two-sample Mendelian Randomization (MR) to examine causal links between plasma lipids, immune cells, and AD. SNPs served as instrumental variables, selected based on GWAS data with significance (P < 1e-5). AD outcomes were sourced from FinnGen, while data on 179 plasma lipids and 731 immune cells came from GWAS. IVW was the main analysis method, with sensitivity tests for heterogeneity and pleiotropy. Mediation MR assessed immune cells as mediators in the liposome-AD pathway, with mediation ratios calculated to quantify their effects. Analyses were conducted in R using the "Two Sample MR" package.
RESULTS: MR analysis identified eight plasma lipids with significant causal associations with AD. Of these, three plasma lipids, including Phosphatidylinositol (16:0_18:1), increased AD risk (OR: 1.61 [1.22 to 2.12], P = .0007), while five others showed protective effects. Analysis revealed 38 immune cell types with causal links to AD, 22 as risk factors and 16 as protective factors. Transitional %B cells mediated 7.9% of the effect between Phosphatidylinositol (16:0_18:1) and AD.
CONCLUSIONS: This study used MR to identify plasma lipids linked to AD, with Phosphatidylinositol (16:0_18:1) showing the strongest effect. While some immune cells (eg, Transitional %B cells) were associated with AD, their mediating role was limited and requires further validation. Future AD prevention should focus on lipid regulation while considering potential immune involvement.
METHODS: This study used two-sample Mendelian Randomization (MR) to examine causal links between plasma lipids, immune cells, and AD. SNPs served as instrumental variables, selected based on GWAS data with significance (P < 1e-5). AD outcomes were sourced from FinnGen, while data on 179 plasma lipids and 731 immune cells came from GWAS. IVW was the main analysis method, with sensitivity tests for heterogeneity and pleiotropy. Mediation MR assessed immune cells as mediators in the liposome-AD pathway, with mediation ratios calculated to quantify their effects. Analyses were conducted in R using the "Two Sample MR" package.
RESULTS: MR analysis identified eight plasma lipids with significant causal associations with AD. Of these, three plasma lipids, including Phosphatidylinositol (16:0_18:1), increased AD risk (OR: 1.61 [1.22 to 2.12], P = .0007), while five others showed protective effects. Analysis revealed 38 immune cell types with causal links to AD, 22 as risk factors and 16 as protective factors. Transitional %B cells mediated 7.9% of the effect between Phosphatidylinositol (16:0_18:1) and AD.
CONCLUSIONS: This study used MR to identify plasma lipids linked to AD, with Phosphatidylinositol (16:0_18:1) showing the strongest effect. While some immune cells (eg, Transitional %B cells) were associated with AD, their mediating role was limited and requires further validation. Future AD prevention should focus on lipid regulation while considering potential immune involvement.