Human Hypertension and Endothelial Cell Activation Promote the Formation and Activation of Axl+ Siglec-6+ Dendritic Cells Via Endothelial Release of Growth Arrest Specific 6
We have shown that dendritic cells (DCs) from hypertensive mice convey hypertension when adoptively transferred to recipients. Recently a novel subset of DCs in humans that express Axl and Sigelc-6+ (AS DCs) have been identified which drive T cell proliferation and produce IL-1β, IL-6 and IL-23, consistent with DCs we have observed in hypertension.
Low fermentable fibre intake has emerged as an important risk factor for hypertension through changes in the gut microbiota, but the biological pathways and specific metabolites involved are unknown.
Endothelial-Derived Microvesicles From Andean Highlanders With Excessive Erythrocytosis Induce a Deleterious Cardiomyocyte Phenotype
Excessive erythrocytosis (EE), defined as Hb ≥21 g/dL in men and ≥19 g/dL in women, is a pathologic consequence of residing at high altitude (>2500 m) and is common in Andean highlanders. EE is associated with increased cardiovascular risk and cardiac dysfunction. Specifically, EE has been linked to congestive heart failure as well as right ventricular hypertrophy in high altitude dwellers.
Expression of Urinary Somatic and Soluble N-Domain Isoforms Of Angiotensin Converting Enzyme and Association With Different Nutritional Status and Cardiovascular Risk Profile
Angiotensin converting enzyme (ACE) plays a dominant role in renal and cardiovascular diseases, obesity and diabetes. The somatic ACE (130-190 kDa) is composed of two homologous N- and C- domains. Two soluble N-domain isoforms have been described in human urine with 65 and 90KDa.
The development of cardiovascular disease in adults has been directly linked to a metabolic phenotype that includes hypertension, obesity and dyslipidemia. While there is evidence that the development of these risk factors in childhood is linked with persistence into adulthood and eventual development of cardiovascular disease, less is known about whether these risk factors contribute to target organ damage during childhood.