Relationship between inflammatory-related cytokines with aortic dissection

Song, Jingjin; Peng, Hua; Lai, Min; Hj, Kang; Chen, X; Cheng, Ye; Su, Xin

doi:10.1016/j.intimp.2023.110618

Cited by 2 publications

(1 citation statement)

References 87 publications

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“…The deposition of fibrinogen, a target of native IgG, was observed to occur prior to the onset of aortic dissection [ 33 ]. This abnormal infiltration of pro-inflammatory cells into the aortic wall subsequently triggered apoptosis of vascular smooth muscle cells (VSMCs) and induced the abnormal expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interferon (IF) [ 34 ]. The apoptotic process of vascular smooth muscle cells (VSMCs) within the medial layer of the vasculature, as well as the dysfunction of VSMCs, are significant factors in the pathogenesis and progression of aortic dissection [ 29 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Qiu,

Liu,

Jiang

et al. 2024

Cardiovasc Diabetol

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Background In observational and experimental studies, diabetes has been reported as a protective factor for aortic dissection. 3-Hydroxybutyrate, a key constituent of ketone bodies, has been found to favor improvements in cardiovascular disease. However, whether the protective effect of diabetes on aortic dissection is mediated by 3-hydroxybutyrate is unclear. We aimed to investigate the causal effects of diabetes on the risk of aortic dissection and the mediating role of 3-hydroxybutyrate in them through two-step Mendelian randomization. Materials and methods We performed a two-step Mendelian randomization to investigate the causal connections between diabetes, 3-hydroxybutyrate, and aortic dissection and calculate the mediating effect of 3-hydroxybutyrate. Publicly accessible data for Type 1 diabetes, Type 2 diabetes, dissection of aorta and 3-hydroxybutyrate were obtained from genome-wide association studies. The association between Type 1 diabetes and dissection of aorta, the association between Type 2 diabetes and dissection of aorta, and mediation effect of 3-hydroxybutyrate were carried out separately. Results The IVW method showed that Type 1 diabetes was negatively associated with the risk of aortic dissection (OR 0.912, 95% CI 0.836–0.995), The weighted median, simple mode and weighted mode method showed consistent results. The mediated proportion of 3-hydroxybutyrate on the relationship between Type 1 diabetes and dissection of aorta was 24.80% (95% CI 5.12–44.47%). The IVW method showed that Type 2 diabetes was negatively associated with the risk of aortic dissection (OR 0.763, 95% CI 0.607–0.960), The weighted median, simple mode and weighted mode method showed consistent results. 3-Hydroxybutyrate does not have causal mediation effect on the relationship between Type 2 diabetes and dissection of aorta. Conclusion Mendelian randomization study revealed diabetes as a protective factor for dissection of aorta. The protective effect of type 1 diabetes on aortic dissection was partially mediated by 3-hydroxybutyrate, but type 2 diabetes was not 3-hydroxybutyrate mediated. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Qiu,

Liu,

Jiang

et al. 2024

Cardiovasc Diabetol

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Correlation of the serum cell division cycle 42 with CD4+ T cell subsets and in-hospital mortality in Stanford type B aortic dissection patients

Peng,

Wang,

Zhang

et al. 2024

Front. Cardiovasc. Med.

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ObjectiveCell division cycle 42 (CDC42) regulates CD4+T-cell differentiation and participates in vascular stiffness and atherosclerosis and is involved in the progression of Stanford type B aortic dissection (TBAD). This study aimed to explore the correlation between serum CDC42 level and CD4+T cell subsets and in-hospital mortality in TBAD patients.MethodsSerum CDC42 and peripheral blood T-helper (Th) 1, Th2, and Th17 cells were detected in 127 TBAD patients by enzyme-linked immunosorbent assay and flow cytometry, respectively. Serum CDC42 was also quantified in 30 healthy controls.ResultsSerum CDC42 was decreased in TBAD patients vs. healthy controls (median [interquartile range (IQR)]: 418.0 (228.0–761.0) pg/ml vs. 992.0 (716.3–1,445.8) pg/ml, P < 0.001). In TBAD patients, serum CDC42 was negatively correlated with Th17 cells (P = 0.001), but not Th1 (P = 0.130) or Th2 cells (P = 0.098). Seven (5.5%) patients experienced in-hospital mortality. Serum CDC42 was reduced in patients who experienced in-hospital mortality vs. those who did not (median (IQR): 191.0 (145.0–345.0) pg/ml vs. 451.5 (298.3–766.8) pg/ml, P = 0.006). By receiver operating characteristic analysis, serum CDC42 showed a good ability for estimating in-hospital mortality [area under curve = 0.809, 95% confidence interval (CI) = 0.662–0.956]. By the multivariate logistic regression analysis, elevated serum CDC42 [odd ratio (OR) = 0.994, 95% CI = 0.998–1.000, P = 0.043] was independently correlated with lower risk of in-hospital mortality, while higher age (OR = 1.157, 95% CI = 1.017–1.316, P = 0.027) was an independent factor for increased risk of in-hospital mortality.ConclusionSerum CDC42 negatively associates with Th17 cells and is independently correlated with decreased in-hospital mortality risk in TBAD patients.

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Relationship between inflammatory-related cytokines with aortic dissection

Cited by 2 publications

References 87 publications

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Diabetes and aortic dissection: unraveling the role of 3-hydroxybutyrate through mendelian randomization

Correlation of the serum cell division cycle 42 with CD4+ T cell subsets and in-hospital mortality in Stanford type B aortic dissection patients

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