Background: Obesity has been linked to arterial stiffness, while no consensus was reached on the association. We aimed to clarify the association of general and central obesity with arterial stiffness by combining observational studies and Mendelian randomization (MR) study.
Methods: Two cross-sectional studies were performed in UK Biobank and Fuqing Cohort, respectively. Two-sample MR study was conducted using summary data of GWASs from GIANT consortium and UK Biobank. General obesity and central obesity were measured using body mass index (BMI) and waist circumference (WC), respectively. Arterial stiffness was measured by arterial stiffness index (ASI) in UK Biobank or branchial-ankle pulse wave velocity (baPWV) in Fuqing Cohort.
Results: Two observational studies found a consistent positive association of BMI and WC with arterial stiffness when adjusting for age, sex, education, smoking, alcohol drinking, physical activity, and LDL cholesterol. However, when additionally adjusting for metabolic traits (i.e., systolic blood pressure, diastolic blood pressure, blood glucose, triglycerides, high-density lipoprotein cholesterol, and WC or BMI), the association with BMI changed to be inverse. As compared to the lowest quintile group, the adjusted ORs across groups of second to fifth quintile were 0.93, 0.90, 0.83, and 0.72 in UK Biobank and 0.88, 0.65, 0.63, and 0.50 in Fuqing Cohort. In contrast, the positive relationship with WC remained stable with the adjusted ORs of 1.23, 1.46, 1.60, and 1.56 in UK Biobank and 1.35, 1.44, 1.77, and 1.64 in Fuqing Cohort. MR analyses provided supportive evidence of the negative association with BMI (OR = 0.97, 95%CI = 0.94-1.00) and the positive association with WC (OR = 1.14, 95%CI = 1.08-1.20).
Conclusions: Observational and genetic analyses provide concordant results that central obesity is independently related to arterial stiffness, while the role of general obesity depends on metabolic status.
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http://dx.doi.org/10.1186/s12916-024-03546-1 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Vascular Biology Center and Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA USA.
The contribution of sex hormones to cardiovascular disease, including arterial stiffness, is established; however, the role of sex chromosome interaction with sex hormones, particularly in women, is lagging. Arterial structural stiffness depends on the intrinsic properties and transmural wall geometry that comprise a network of cells and extracellular matrix (ECM) proteins expressed in a sex-dependent manner. In this study, we used four-core genotype (FCG) mice to determine the relative contribution of sex hormones versus sex chromosomes or their interaction with arterial structural stiffness.
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Department of Vascular Surgery, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
Downregulated RhoA/ROCK1/YAP/F-actin axis leads to decreased AoSMC stiffness and promotes AD formation.
View Article and Find Full Text PDFIn Vitro Model
February 2024
Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of Science and Technology (BIST), Barcelona, Spain.
Unlabelled: Neuroblastoma (NB) is a highly vascularized pediatric tumor arising from undifferentiated neural crest cells early in life, exhibiting both traditional endothelial-cell-driven vasculature and an intriguing alternative vasculature. The alternative vasculature can arise from cancer cells undergoing transdifferentiation into tumor-derived endothelial cells (TEC), a trait associated with drug resistance and tumor relapse. The lack of effective treatments targeting NB vasculature primarily arises from the challenge of establishing predictive in vitro models that faithfully replicate the alternative vasculature phenomenon.
View Article and Find Full Text PDFIntroduction: Several anthropometric indices reflecting cardiometabolic risks have been developed, but the relationship of body composition with arterial stiffness remains unclear. We aimed to determine the interaction between age-related anthropometric changes and progression of arterial stiffness.
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Lymphat Res Biol
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Department of Plastic and Reconstructive Surgery, Medical Centre of Postgraduate Education, Warsaw, Poland.
Upper limb lymphedema is the most common complication after breast cancer therapy. Suddenly disturbed lymphatic transport in the affected arm causes tissue fluid accumulation in tissue spaces, limb enlargement, and secondary changes in tissue. Early compression therapy is necessary.
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