Vascular Dysfunction Research Articles

Quercetin protects red blood cells from aggregation, eryptosis, and delayed hemolysis caused by cell-free histones through sialic acid interaction.

Quercetin protects red blood cells from aggregation, eryptosis, and delayed hemolysis caused by cell-free histones through sialic acid interaction.

Hypoxia in multiple sclerosis.

Hypoxia in multiple sclerosis.

Irisin alleviates steroid-induced vascular dysfunction by regulating the αVβ5-c-Abl-Caveolin-1 signaling pathway.

Irisin alleviates steroid-induced vascular dysfunction by regulating the αVβ5-c-Abl-Caveolin-1 signaling pathway.

Unravelling soluble (pro)renin receptor-mediated endothelial dysfunction.

Unravelling soluble (pro)renin receptor-mediated endothelial dysfunction.

Increasing nitric oxide availability via ingestion of nitrate-rich beetroot juice improves vascular responsiveness in individuals with Alzheimer's Disease.

Increasing nitric oxide availability via ingestion of nitrate-rich beetroot juice improves vascular responsiveness in individuals with Alzheimer's Disease.

Copper exposure at a daily dose twice the recommended in diabetic rats induces oxidative stress, vascular dysfunction and perivascular adipose tissue inflammation in diabetic rats.

Copper exposure at a daily dose twice the recommended in diabetic rats induces oxidative stress, vascular dysfunction and perivascular adipose tissue inflammation in diabetic rats.

Epigallocatechin-3-gallate as an effective inhibitor of vascular endothelial dysfunction induced by endothelial-localized myeloperoxidase.

Epigallocatechin-3-gallate as an effective inhibitor of vascular endothelial dysfunction induced by endothelial-localized myeloperoxidase.

Nitric oxide mediates negative feedback on the TXNIP/NLRP3 inflammasome pathway to prevent retinal neurovascular unit dysfunction in early diabetic retinopathy.

Nitric oxide mediates negative feedback on the TXNIP/NLRP3 inflammasome pathway to prevent retinal neurovascular unit dysfunction in early diabetic retinopathy.

Endothelial Stiffening Induced by CD36-Mediated Lipid Uptake Leads to Endothelial Barrier Disruption and Contributes to Atherosclerotic Lesions.

Endothelial stiffening induced by Western diet was proposed to be an important factor in vascular dysfunction. In this study, we determine the role of endothelial CD36 (cluster of differentiation 36) in stiffening, disruption of aortic endothelial barrier, and atherosclerosis in mouse models of obesity and hypercholesterolemia. To address this goal, we generated an endothelial-specific inducible knockdown mouse model of CD36, Cdh5.CreERT2CD36fl/fl, on C57/BL6J wild-type and LDLR-/- genetic backgrounds. Endothelial stiffness is assessed by atomic force microscopy; endothelial barrier integrity is assessed by imaging VE-cadherin junctions and by penetration of Evans blue dye into the aortic wall. Atherosclerotic plaques are quantified using oil red O staining. Endothelial-specific downregulation of CD36 abrogates stiffening of aortic endothelium induced by Western diet in Cdh5.CreERT2CD36fl/fl and in Cdh5.CreERT2CD36fl/flLDLR-/- mice. Prevention of Western diet-induced endothelial stiffening by downregulation of CD36 is associated with a protective effect against endothelial barrier disruption in both mouse models and with a significant decrease in the areas of atherosclerotic lesions in Cdh5.CreERT2CD36fl/flLDLR-/- mice. Mechanistically, stiffening of human aortic endothelial cells in vitro is induced by saturated fatty acids, particularly palmitic acid (PA), which results in activation of RhoA. Both PA-induced endothelial stiffening and RhoA activation are abrogated by CD36 siRNA. Furthermore, PA-induced endothelial stiffening of excised aortas ex vivo is lost in aortas isolated from mice, where endothelial CD36 is downregulated. We also demonstrate that PA-induced activation of RhoA and endothelial stiffening require expressing an RhoA-inhibitory protein, Rho-GDI1 (Rho guanosine dissociation inhibitor 1). Finally, we discover that PA disrupts the colocalization of RhoA with Rho-GDI1. We conclude that stiffening of the aortic endothelium by CD36-mediated uptake of fatty acids contributes significantly to Western diet-induced vascular dysfunction and atherosclerosis. We further propose that fatty acids may activate RhoA by inducing its dissociation from Rho-GDI1.

Toward a rational therapeutic for elastin related disease: Key considerations for elastin based regenerative medicine strategies.

Toward a rational therapeutic for elastin related disease: Key considerations for elastin based regenerative medicine strategies.

Malvidin-3-O-glucoside ameliorates the development of vascular endothelial dysfunction in type 2 diabetes mellitus by inhibiting arginase 1 expression

Malvidin-3-O-glucoside ameliorates the development of vascular endothelial dysfunction in type 2 diabetes mellitus by inhibiting arginase 1 expression

MiR-34a-5p/MARCHF8/ADAM10 axis in the regulation of vascular endothelial cell dysfunction and senescence.

miR-34a-5p/MARCHF8/ADAM10 axis in the regulation of vascular endothelial cell dysfunction and senescence.

O6-methylguanine-DNA methyltransferase inhibition leads to cellular senescence and vascular smooth muscle dysfunction.

O6-methylguanine-DNA methyltransferase inhibition leads to cellular senescence and vascular smooth muscle dysfunction.

Exploring the connection between dementia and cardiovascular risk with a focus on ADAM10.

Exploring the connection between dementia and cardiovascular risk with a focus on ADAM10.

Melatonin ameliorates retinal neurovascular degeneration in Rd1 mice by inhibiting oxidativestress.

Melatonin ameliorates retinal neurovascular degeneration in Rd1 mice by inhibiting oxidativestress.

LncRNAs in vascular senescence and microvascular remodeling.

Long noncoding RNAs (lncRNAs) have emerged as critical regulators of vascular senescence and microvascular remodeling, processes that significantly contribute to the development of age-related diseases in organs such as the kidneys, heart, and lungs. Through mechanisms like chromatin remodeling, transcriptional regulation, and posttranscriptional modifications, lncRNAs modulate gene expression, thereby influencing cellular processes such as apoptosis, inflammation, fibrosis, and angiogenesis. In chronic kidney disease, cardiovascular disease, and pulmonary disorders, lncRNAs play a central role in promoting vascular dysfunction, endothelial cell aging, and fibrosis. This review focuses on how lncRNAs contribute to endothelial dysfunction, fibrosis, and vascular aging, emphasizing their roles in disease progression within the kidneys, heart, and lungs, where lncRNA-mediated vascular changes play a significant role in disease progression. Understanding the interactions between lncRNAs, vascular senescence, and microvascular remodeling offers promising avenues for developing targeted therapeutic strategies to mitigate the impact of aging on vascular health.

Update in the molecular mechanism and biomarkers of diabetic retinopathy.

Update in the molecular mechanism and biomarkers of diabetic retinopathy.

Endogenous acrolein accumulation in akr7a3 mutants causes microvascular dysfunction due to increased arachidonic acid metabolism.

Endogenous acrolein accumulation in akr7a3 mutants causes microvascular dysfunction due to increased arachidonic acid metabolism.

Metabolic and vascular insulin resistance: partners in the pathogenesis of cardiovascular disease in diabetes.

Vascular insulin resistance has emerged as a pivotal factor in the genesis of cardiovascular disease (CVD) in people with diabetes. It forms a complex pathogenic partnership with metabolic insulin resistance to significantly amplify the CVD risk of diabetes and other affected populations. Metabolic insulin resistance (characterized by quantitatively diminished insulin action on glucose metabolism in skeletal muscle, liver, and adipose tissue) is a hallmark of diabetes, obesity, and related conditions. In contrast, vascular insulin resistance is a less appreciated and not well-quantified complication of these conditions. Importantly, an impaired vascular response to insulin contributes directly to vascular dysfunction and over 40 years of research has convincingly shown that vascular and metabolic insulin resistance synergize to create an environment that predisposes individuals to CVD. In this review, we examine the multifaceted vascular actions of insulin, including its roles in regulating blood pressure, blood flow, endothelial health, and arterial stiffness. We also examine how these processes become disrupted in the setting of vascular insulin resistance, which subsequently undermines endothelial function, compromises tissue microvascular perfusion, and promotes vascular rigidity and atherosclerosis. We then highlight potential therapeutic strategies with demonstrated efficacy to improve vascular insulin sensitivity in people with diabetes and suggest that targeting disordered vascular insulin signaling holds promise not only for refining the functional understanding of vascular insulin resistance but also for developing innovative treatments with potential to reduce CVD risk and improve cardiovascular outcomes in people with diabetes.

Elevated Trimethylamine-N-oxide (TMAO) Is Associated with Vascular Access Dysfunction in Maintenance Hemodialysis Patients.

Elevated levels of trimethylamine-N-oxide (TMAO), a metabolite produced by gut microbiota, have been associated with cardiovascular diseases and complications in various populations. However, its role in vascular access dysfunction in hemodialysis patients remains underexplored. This study investigates the potential relationship between TMAO levels and vascular access dysfunction in maintenance hemodialysis patients. This study included 80 hemodialysis patients. The baseline serum TMAO levels were measured, and clinical characteristics and dialysis-related data were collected. They were followed up on vascular access dysfunction events over a period of 1 year. The association between serum TMAO levels and vascular access dysfunction events were investigated. In our cohort, we observed a wide distribution of serum concentrations, with a median concentration of 15.2 μmol/L and a maximum concentration of 245.3 μmol/L. Patients were stratified into a low-TMAO group and a high-TMAO group according to the median value of TMAO concentrations. Those in the high-TMAO group had a significantly higher incidence of vascular access dysfunction events (p = 0.023). TMAO was independently associated with vascular access dysfunction events after adjusting for some potential vascular access dysfunction risk factors. This study suggests that elevated serum TMAO levels may serve as an independent risk factor for vascular access dysfunction in hemodialysis patients. Reducing TMAO levels may potentially decrease the incidence of vascular access dysfunction, warranting further investigation into this therapeutic approach.