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Cinnamic acid alleviates endothelial dysfunction and oxidative stress by targeting PPARδ in obesity and diabetes.
Chin Med
January 2025
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao SAR, China.
Objective: Cinnamic acid (CA) is a bioactive compound isolated from cinnamon. It has been demonstrated to ameliorate inflammation and metabolic diseases, which are associated with endothelial dysfunction. This study was aimed to study the potential protective effects of CA against diabetes-associated endothelial dysfunction and its underlying mechanisms.
View Article and Find Full Text PDFThe lncRNA DSCR9 is modulated in pulmonary arterial hypertension endothelial cell models and is associated with alterations in the nitric oxide pathway.
Vascul Pharmacol
January 2025
Department of Internal Medicine, University of Genova, Genova, Italy; IRCCS Ospedale Policlinico San Martino, Genova, Italy. Electronic address:
Long non-coding RNA (lncRNA) may be involved in dysfunction of pulmonary artery endothelial cells (PAEC) and, thus, in pulmonary arterial hypertension (PAH) pathobiology. We screened the RNA expression profile of commercial human PAEC (hPAEC) exposed to increased hydrostatic pressure, and found that the lncRNA Down syndrome critical region 9 (DSCR9) was the most regulated transcript (log2FC 1.89 vs control).
View Article and Find Full Text PDFMFN2-mediated decrease in mitochondria-associated endoplasmic reticulum membranes contributes to sunitinib-induced endothelial dysfunction and hypertension.
J Mol Cell Cardiol
January 2025
Department of Cardiology, Harbin Medical University Cancer Hospital, NHC Key Laboratory of Cell Transplantation, Department of Cardiology, Central Laboratory, The First Affiliated Hospital of Harbin Medical University, Institute of Metabolic Disease, Heilongjiang Academy of Medical Sciences, Heilongjiang Key Laboratory for Metabolic Disorder & Cancer Related Cardiovascular Diseases, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin, China. Electronic address:
Unlabelled: Treatment of cancer patients with tyrosine kinase inhibitors (TKIs) often results in hypertension, but the underlying mechanism remains unclear. This study aimed to examine the role of mitochondrial morphology and function, particularly mitochondria-associated endoplasmic reticulum membranes (MAMs), in sunitinib-induced hypertension.
Methods: Both in vitro and in vivo experiments performed to assesse reactive oxygen species (ROS), nitric oxide (NO), endothelium-dependent vasorelaxation, systemic blood pressure, and mitochondrial function in human umbilical vein endothelial cells (HUVECs) and C57BL/6 mouse aortic endothelial cells, under vehicle or sunitinib treatment condition.
Association studies of vasoactive genes and preeclampsia in taiwan.
Placenta
January 2025
Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan City, Taiwan. Electronic address:
Background: Preeclampsia (PE) is a serious condition characterized by hypertension and proteinuria after 20 weeks of gestation. The exact cause of PE is unknown but may involve abnormalities in the renin-angiotensin-aldosterone system (RAAS) and endothelial nitric oxide synthase (eNOS). Genetic variations in angiotensinogen (AGT), angiotensin-converting enzyme (ACE), and eNOS genes have been associated with PE.
View Article and Find Full Text PDFUnraveling the molecular complexity of bicuspid aortopathy: Lessons from comparative proteomics.
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Animal Biology, Faculty of Science, University of Málaga, Málaga, Spain; Biomedical Research Institute of Málaga and Platform on Nanomedicine (IBIMA-Plataforma BIONAND), Málaga, Spain; Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Molecular markers and pathways involved in the etiology and pathophysiology of bicuspid aortopathy are poorly understood. The aim here is to delve into the molecular and cellular mechanisms of the disease and identify potential predictive molecular markers using a well-established isogenic hamster model (T-strain) of bicuspid aortic valve (BAV) and thoracic aortic dilatation (TAD). We carried out comparative quantitative proteomics combined with western blot and morpho-molecular analyses in the ascending aorta of tricuspid aortic valve (TAV) and BAV animals from the T-strain, and TAV animals from a control strain.
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