scholarly journals Atorvastatin protects against liver and vascular damage in a model of diet induced steatohepatitis by resetting FXR and GPBAR1 signaling

2021 ◽  
Vol 36 (1) ◽  
Author(s):  
Silvia Marchianò ◽  
Michele Biagioli ◽  
Rosalinda Roselli ◽  
Angela Zampella ◽  
Cristina Di Giorgio ◽  
...  
Keyword(s):  
Vascular Damage

Targeting the Endothelial Ca2+ Toolkit to Rescue Endothelial Dysfunction in Obesity Associated-Hypertension

2020 ◽  
Vol 27 (2) ◽  
pp. 240-257 ◽  
Author(s):  
Francesco Moccia ◽  
Sharon Negri ◽  
Pawan Faris ◽  
Roberto Berra-Romani
Keyword(s):  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Endothelial Damage ◽  
Vascular Damage ◽  
Zucker Rats ◽  
Bibliographic Databases ◽  
Resistance Arteries ◽  
Small Resistance ◽  
Obese Zucker Rats ◽  
Transient Receptor

Background: Obesity is a major cardiovascular risk factor which dramatically impairs endothelium- dependent vasodilation and leads to hypertension and vascular damage. The impairment of the vasomotor response to extracellular autacoids, e.g., acetylcholine, mainly depends on the reduced Nitric Oxide (NO) bioavailability, which hampers vasorelaxation in large conduit arteries. In addition, obesity may affect Endothelium-Dependent Hyperpolarization (EDH), which drives vasorelaxation in small resistance arteries and arterioles. Of note, endothelial Ca2+ signals drive NO release and trigger EDH. Methods: A structured search of bibliographic databases was carried out to retrieve the most influential, recent articles on the impairment of vasorelaxation in animal models of obesity, including obese Zucker rats, and on the remodeling of the endothelial Ca2+ toolkit under conditions that mimic obesity. Furthermore, we searched for articles discussing how dietary manipulation could be exploited to rescue Ca2+-dependent vasodilation. Results: We found evidence that the endothelial Ca2+ could be severely affected by obese vessels. This rearrangement could contribute to endothelial damage and is likely to be involved in the disruption of vasorelaxant mechanisms. However, several Ca2+-permeable channels, including Vanilloid Transient Receptor Potential (TRPV) 1, 3 and 4 could be stimulated by several food components to stimulate vasorelaxation in obese individuals. Conclusion: The endothelial Ca2+ toolkit could be targeted to reduce vascular damage and rescue endothelium- dependent vasodilation in obese vessels. This hypothesis remains, however, to be probed on truly obese endothelial cells.

Immune System Alterations by Aldosterone During Hypertension: From Clinical Observations to Genomic and Non-Genomic Mechanisms Leading to Vascular Damage

2013 ◽  
Vol 13 (6) ◽  
pp. 1035-1046 ◽  
Author(s):  
N. Munoz-Durango ◽  
M.F. Barake ◽  
N.A. Letelier ◽  
C. Campino ◽  
C.E. Fardella ◽  
...  
Keyword(s):  
Immune System ◽  
Vascular Damage ◽  
Clinical Observations

Sympathetic drive and vascular damage in hypertension and atherosclerosis.

Hypertension ◽  
1991 ◽  
Vol 17 (4_Suppl) ◽  
pp. III75-III75 ◽  
Author(s):  
P. Pauletto ◽  
G. Scannapieco ◽  
A. C. Pessina
Keyword(s):  
Vascular Damage

scholarly journals Colonization of dermal arterioles by Neisseria meningitidis provides a safe haven from neutrophils

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Valeria Manriquez ◽  
Pierre Nivoit ◽  
Tomas Urbina ◽  
Hebert Echenique-Rivera ◽  
Keira Melican ◽  
...  
Keyword(s):  
Neisseria Meningitidis ◽  
Inflammatory Infiltrate ◽  
Immune Escape ◽  
Systemic Disease ◽  
Neutrophil Recruitment ◽  
Vascular Damage ◽  
Bacterial Burden ◽  
Human Pathogen ◽  
Humanized Mouse ◽  
Humanized Mouse Model

AbstractThe human pathogen Neisseria meningitidis can cause meningitis and fatal systemic disease. The bacteria colonize blood vessels and rapidly cause vascular damage, despite a neutrophil-rich inflammatory infiltrate. Here, we use a humanized mouse model to show that vascular colonization leads to the recruitment of neutrophils, which partially reduce bacterial burden and vascular damage. This partial effect is due to the ability of bacteria to colonize capillaries, venules and arterioles, as observed in human samples. In venules, potent neutrophil recruitment allows efficient bacterial phagocytosis. In contrast, in infected capillaries and arterioles, adhesion molecules such as E-Selectin are not expressed on the endothelium, and intravascular neutrophil recruitment is minimal. Our results indicate that the colonization of capillaries and arterioles by N. meningitidis creates an intravascular niche that precludes the action of neutrophils, resulting in immune escape and progression of the infection.

scholarly journals AB0026 DECREASE OF ANGIOGENIC T CELLS IN CONNECTIVE TISSUE DISEASE-ASSOCIATED INTERSTITIAL LUNG DISEASE

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1046.3-1047
Author(s):  
V. Pulito-Cueto ◽  
S. Remuzgo Martinez ◽  
F. Genre ◽  
B. Atienza-Mateo ◽  
V. M. Mora-Cuesta ◽  
...  
Keyword(s):  
T Cells ◽  
Interstitial Lung Disease ◽  
Connective Tissue ◽  
Lung Disease ◽  
Cell Subset ◽  
Vascular Damage ◽  
Type I ◽  
Research Support ◽  
Angiogenic T Cells

Background:Interstitial lung disease (ILD) is one of the most significant complications of connective tissue diseases (CTD), leading to an increase of the morbidity and mortality in patients with CTD [1]. A specific T cell subset termed angiogenic T cells (TAng), that promote endothelial repair and revascularization, have been involved in the pathogenesis of CTD [2-4]. However, to the best of our knowledge, no information regarding the role of TAng in CTD-ILD+ is available.Objectives:To study, for the first time, the potential role of TAng related to vascular damage in CTD-ILD+.Methods:Peripheral venous blood was collected from 40 patients with CTD-ILD+ and three comparative groups: 44 CTD-ILD- patients, 21 idiopathic pulmonary fibrosis (IPF) patients and 20 healthy controls (HC). All subjects were recruited from the Rheumatology and Pneumology departments of Hospital Universitario Marqués de Valdecilla, Santander, Spain. Quantification of TAng was performed by flow cytometry. TAng were considered as triple-positive for CD3, CD31 and CXCR4.Results:Patients with CTD-ILD+ exhibited a significantly lower TAng frequency than CTD-ILD- patients (p<0.001). Similar results were obtained when patients with CTD-ILD+ were compared with HC (p=0.004) although no difference was observed between CTD-ILD+ and IPF. In addition, a significant increase of TAng frequency was shown in patients with CTD-ILD- in relation to IPF patients (p<0.001), while no difference was observed between CTD-ILD- and HC.Conclusion:Our results reveal a decrease of TAng frequency related to vascular damage in CTD-ILD+. Furthermore, we disclose that the presence of ILD is associated with lower TAng frequency.References:[1]Expert Rev Clin Immunol 2018;14(1):69-82.[2]Circulation 2007;116(15):1671-82.[3]Ann Rheum Dis 2015 74(5):921-7.[4]PLoS One 2017;12(8):e0183102.Acknowledgements:Personal funds, VP-C: PREVAL18/01 (IDIVAL); SR-M: RD16/0012/0009 (ISCIII-ERDF); LL-G: INNVAL20/06 (IDIVAL); RP-F: START PROJECT (FOREUM); RL-M: Miguel Servet type I CP16/00033 (ISCIII-ESF).Disclosure of Interests:Verónica Pulito-Cueto: None declared, Sara Remuzgo Martinez: None declared, Fernanda Genre: None declared, Belén Atienza-Mateo: None declared, Victor Manuel Mora-Cuesta: None declared, David Iturbe-Fernández: None declared, Leticia Lera-Gómez: None declared, Raquel Pérez-Fernández: None declared, Pilar Alonso Lecue: None declared, Javier Rodriguez Carrio: None declared, Diana Prieto-Peña: None declared, Virginia Portilla: None declared, Ricardo Blanco Speakers bureau: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Consultant of: Abbvie, Pfizer, Roche, Bristol-Myers, Janssen and MSD, Grant/research support from: Abbvie, MSD and Roche, Alfonso Corrales: None declared, Jose Manuel Cifrián-Martínez: None declared, Raquel López-Mejías: None declared, Miguel A González-Gay Speakers bureau: Pfizer, Abbvie, MSD, Grant/research support from: Pfizer, Abbvie, MSD

Profile of new vascular damage biomarkers in middle-aged men with arterial hypertension

2021 ◽  
Vol 66 (1) ◽  
pp. 185-191
Author(s):  
Angelika Edyta Charkiewicz ◽  
Marzena Garley ◽  
Wioletta Ratajczak-Wrona ◽  
Karolina Nowak ◽  
Ewa Jabłońska ◽  
...  
Keyword(s):  
Arterial Hypertension ◽  
Vascular Damage ◽  
Middle Aged
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