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Abstract The triglyceride glucose‐body mass index (TyG‐BMI) has been considered an alternative marker of insulin resistance (IR). This cross‐sectional study was designed to mainly investigate the association between TyG‐BMI, triglyceride glucose combined with body mass index, and hypertension in Chinese adults. The relationship between TyG‐BMI and hypertension was examined by multivariate logistic regression and restricted cubic spline model. Multiple logistic regression models were also performed to examine the associations between the individual components of TyG‐BMI (BMI, TyG index, TG and FBG) and hypertension. The incremental ability of TyG‐BMI versus its individual components for hypertension discrimination was evaluated by C‐statistic and net reclassification index. Subgroup analysis was performed to examine potential interactions. A total of 92,545 participants (38.9% men, mean age 53.7 years) were included for final analysis. Logistic regression models showed TyG‐BMI and its individual components were all significantly associated with the odds of hypertension (p for trend

Abstract Development of abdominal aortic aneurysms (AAA) enhances lesion group‐2 innate lymphoid cell (ILC2) accumulation and blood IL5. ILC2 deficiency in Rorafl/flIl7rCre/+ mice or induced ILC2 depletion in Icosfl‐DTR‐fl/+Cd4Cre/+ mice expedites AAA growth, increases lesion inflammation, but leads to systemic IL5 and eosinophil (EOS) deficiency. Mechanistic studies show that ILC2 protect mice from AAA formation via IL5 and EOS. IL5 or ILC2 from wild‐type (WT) mice, but not ILC2 from Il5−/− mice induces EOS differentiation in bone‐marrow cells from Rorafl/flIl7rCre/+ mice. IL5, IL13, and EOS or ILC2 from WT mice, but not ILC2 from Il5−/− and Il13−/− mice block SMC apoptosis and promote SMC proliferation. EOS but not ILC2 from WT or Il5−/− mice block endothelial cell (EC) adhesion molecule expression, angiogenesis, dendritic cell differentiation, and Ly6Chi monocyte polarization. Reconstitution of WT EOS and ILC2 but not Il5−/− ILC2 slows AAA growth in Rorafl/flIl7rCre/+ mice by increasing systemic EOS. Besides regulating SMC pathobiology, ILC2 play an indirect role in AAA protection via the IL5 and EOS mechanism.