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Receptors for the vasoactive adipokine apelin, termed APJ receptors, are G-protein-coupled receptors and are widely expressed throughout the cardiovascular system. APJ receptors can also signal via G-protein-independent pathways, including G-protein-coupled-receptor kinase 2 (GRK2), which inhibits nitric oxide synthase (eNOS) activity and nitric oxide (NO) production in endothelial cells. Apelin causes endothelium-dependent, NO-mediated relaxation of coronary arteries from normotensive animals, but the effects of activating APJ receptor signaling pathways in hypertensive coronary arteries are largely unknown.
View Article and Find Full Text PDFKlebsiella pneumoniae-derived extracellular vesicles impair endothelial function by inhibiting SIRT1.
Cell Commun Signal
January 2025
Beijing An Zhen Hospital, Capital Medical University, The Key Laboratory of Remodeling Cardiovascular Diseases, Ministry of Education; Collaborative Innovation Center for Cardiovascular Disorders, Beijing Institute of Heart Lung and Blood Vessel Disease, Beijing, 100029, China.
Background: The potential role of Klebsiella pneumoniae (K.pn) in hypertension development has been emphasized, although the specific mechanisms have not been well understood. Bacterial extracellular vesicles (BEVs) released by Gram-negative bacteria modulate host cell functions by delivering bacterial components to host cells.
View Article and Find Full Text PDFBisphenol S induced endothelial dysfunction via mitochondrial pathway in the vascular endothelial cells, and detoxification effect of albumin binding.
Chem Biol Interact
January 2025
College of Chemistry and Materials, Key Laboratory of Green Catalysis of Jiangxi Education Institutes, Jiangxi Normal University, Nanchang, 330022, China. Electronic address:
As a replacement of bisphenol A, bisphenol S (BPS) is commonly used in the wrappers and food containers of daily life. Epidemiological studies demonstrate a close link between BPS exposure and vascular diseases, where the biological activities of BPS remain scarcely known. Herein, the effects of BPS on endothelial function as well as the underlying mechanism were investigated in human umbilical vein endothelial cells (HUVECs) and mouse arteries.
View Article and Find Full Text PDFImpaired cerebral microvascular reactivity and endothelial SK channel activity in a streptozotocin-treated mouse model of Alzheimer's disease.
J Alzheimers Dis
January 2025
Division of Cardiothoracic Surgery, Rhode Island Hospital, Alpert Medical School of Brown University, Providence, RI, USA.
Article Synopsis
- Alzheimer's disease (AD) is characterized by various pathological features including amyloid-β deposition and tau hyperphosphorylation, with cerebral microvascular dysfunction likely playing a role in its progression.
- Researchers investigated the microvascular responses and potassium channel activity in an AD mouse model induced by streptozotocin (STZ), using behavioral tests and cellular assays.
- The study found that STZ-AD mice showed poorer performance on behavioral tests and had impaired microvascular responses, which were further deteriorated by exposure to soluble Aβ, indicating a potential link between microvascular dysfunction and AD pathology.
Angiotensin II Exposure In Vitro Reduces High Salt-Induced Reactive Oxygen Species Production and Modulates Cell Adhesion Molecules' Expression in Human Aortic Endothelial Cell Line.
Biomedicines
November 2024
Department of Physiology and Immunology, Faculty of Medicine Osijek, J. J. Strossmayer University of Osijek, J. Huttlera 4, 31000 Osijek, Croatia.
: Increased sodium chloride (NaCl) intake led to leukocyte activation and impaired vasodilatation via increased oxidative stress in human/animal models. Interestingly, subpressor doses of angiotensin II (AngII) restored endothelium-dependent vascular reactivity, which was impaired in a high-salt (HS) diet in animal models. Therefore, the present study aimed to assess the effects of AngII exposure following high salt (HS) loading on endothelial cells' (ECs') viability, activation, and reactive oxygen species (ROS) production.
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