Endothelial dysfunction is one of the major diabetic complications causing morbidity and mortality of large number of patients. Oxidative stress is key factor in the development and progression of such pathological changes. Hyperglycaemia and/or hyperlipidaemia accompanying diabetes, cause increased production of reactive oxygen species in parallel with significantly reduced antioxidative defence. The vascular endothelium is not only passive lining of the vessels but also highly metabolically active tissue. It produces and secretes a number of factors responsible for the maintenance of vascular homeostasis. Oxidative stress leads to changes in vascular tone, which mainly involves the reduction of NO bioavailability. There are several ROS generating mechanisms, however it seems that the mitochondrial respiratory chain and NAD(P)H oxidase play a most significant role in endothelium. The endothelial dysfunction in diabetes, the importance of mitochondria and NAD(P)H oxidase in the development of pathological changes would be discussed below.
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Sci Adv
January 2025
Division of Regenerative Medicine, Hartman Institute for Therapeutic Organ Regeneration, Ansary Stem Cell Institute, Department of Medicine, Weill Cornell Medicine, New York, NY, USA.
Tissue-specific endothelial cells (ECs) are critical for the homeostasis of pancreatic islets and most other tissues. In vitro recapitulation of islet biology and therapeutic islet transplantation both require adequate vascularization, which remains a challenge. Using human reprogrammed vascular ECs (R-VECs), human islets were functionally vascularized in vitro, demonstrating responsive, dynamic glucose-stimulated insulin secretion and Ca influx.
View Article and Find Full Text PDFClin Sci (Lond)
January 2025
Center for Interdisciplinary Research in Biology, College de France, Institut National de la Santé et de la Recherche Médicale, Paris, France.
Apelin, a (neuro) vasoactive peptide, plays a prominent role in controlling water balance and cardiovascular functions. Apelin and its receptor co-localize with vasopressin in magnocellular vasopressinergic neurons. Apelin receptors (Apelin-Rs) are also expressed in the collecting ducts of the kidney, where vasopressin type 2 receptors are also present.
View Article and Find Full Text PDFPhysiol Rep
February 2025
Department of Biomedical Engineering, Toyo University, Saitama, Japan.
The present study aims to examine the effect of 4 h of continuous sitting on cerebral endothelial function, which is a crucial component of cerebral blood flow regulation. We hypothesized that 4 h of sitting may impair cerebral endothelial function similarly to how it affects lower limb vasculature. Thirteen young, healthy participants were instructed to remain seated for 4 h without moving their lower limbs.
View Article and Find Full Text PDFInt Angiol
December 2024
Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA -
The glycocalyx is an essential structural and functional component of endothelial cells. Extensive hemodynamic changes cause endothelial glycocalyx disruption and vascular dysfunction, leading to multiple arterial and venous disorders. Chronic venous disease (CVD) is a common disorder of the lower extremities with major health and socio-economic implications, but complex pathophysiology.
View Article and Find Full Text PDFJ Ginseng Res
January 2025
The Key Laboratory of Cardiovascular and Cerebrovascular Drug Research of Liaoning Province, Jinzhou Medical University, Jinzhou, China.
Background: Vascular endothelial dysfunction (VED) is one of the main pathogenic events in pulmonary arterial hypertension (PAH). Previous studies have demonstrated that the ginsenoside Rg1 (Rg1) can ameliorate PAH, but the mechanism by which Rg1 affects pulmonary VED in hypoxia-induced PAH remains unclear.
Methods: Network pharmacology, molecular docking and other experiments were used to explore the mechanisms by which Rg1 affects PAH.
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