scholarly journals Hutchinson-Gilford progeria syndrome, cardiovascular disease and oxidative stress

10.2741/226 ◽  
2011 ◽  
Vol S3 (1) ◽  
pp. 1285 ◽  
Author(s):  
Laia Trigueros-Motos
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome ◽  
And Oxidative Stress

scholarly journals Cardiovascular Disease-Related Parameters and Oxidative Stress in SHROB Rats, a Model for Metabolic Syndrome

PLoS ONE ◽  
2014 ◽  
Vol 9 (8) ◽  
pp. e104637 ◽  
Author(s):  
Eunice Molinar-Toribio ◽  
Jara Pérez-Jiménez ◽  
Sara Ramos-Romero ◽  
Laura Lluís ◽  
Vanessa Sánchez-Martos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Metabolic Syndrome ◽  
And Oxidative Stress

The opposing roles of NO and oxidative stress in cardiovascular disease

2017 ◽  
Vol 116 ◽  
pp. 57-69 ◽  
Author(s):  
Rebecca H. Ritchie ◽  
Grant R. Drummond ◽  
Christopher G. Sobey ◽  
T. Michael De Silva ◽  
Barbara K. Kemp-Harper
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
And Oxidative Stress

scholarly journals New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 529 ◽  
Author(s):  
Hénaut ◽  
Candellier ◽  
Boudot ◽  
Grissi ◽  
Mentaverri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cellular Interactions ◽  
Valvular Interstitial Cells ◽  
Macrophage Subset ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines ◽  
Valvular Cells

Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.

scholarly journals A pathway linking oxidative stress and the Ran GTPase system in progeria

2014 ◽  
Vol 25 (8) ◽  
pp. 1202-1215 ◽  
Author(s):  
Sutirtha Datta ◽  
Chelsi J. Snow ◽  
Bryce M. Paschal
Keyword(s):  
Oxidative Stress ◽  
Nuclear Membrane ◽  
Nucleocytoplasmic Transport ◽  
Lamin A ◽  
Mutant Form ◽  
Ran Gtpase ◽  
Nuclear Levels ◽  
Progeria Syndrome ◽  
Hutchinson Gilford Progeria Syndrome ◽  
The Relationship

Maintaining the Ran GTPase at a proper concentration in the nucleus is important for nucleocytoplasmic transport. Previously we found that nuclear levels of Ran are reduced in cells from patients with Hutchinson–Gilford progeria syndrome (HGPS), a disease caused by constitutive attachment of a mutant form of lamin A (termed progerin) to the nuclear membrane. Here we explore the relationship between progerin, the Ran GTPase, and oxidative stress. Stable attachment of progerin to the nuclear membrane disrupts the Ran gradient and results in cytoplasmic localization of Ubc9, a Ran-dependent import cargo. Ran and Ubc9 disruption can be induced reversibly with H2O2. CHO cells preadapted to oxidative stress resist the effects of progerin on Ran and Ubc9. Given that HGPS-patient fibroblasts display elevated ROS, these data suggest that progerin inhibits nuclear transport via oxidative stress. A drug that inhibits pre–lamin A cleavage mimics the effects of progerin by disrupting the Ran gradient, but the effects on Ran are observed before a substantial ROS increase. Moreover, reducing the nuclear concentration of Ran is sufficient to induce ROS irrespective of progerin. We speculate that oxidative stress caused by progerin may occur upstream or downstream of Ran, depending on the cell type and physiological setting.

scholarly journals Dislipidemia and oxidative stress in mild and in severe psoriasis as a risk for cardiovascular disease

2001 ◽  
Vol 303 (1-2) ◽  
pp. 33-39 ◽  
Author(s):  
Petronila Rocha-Pereira ◽  
Alice Santos-Silva ◽  
Irene Rebelo ◽  
Américo Figueiredo ◽  
Alexandre Quintanilha ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Severe Psoriasis ◽  
And Oxidative Stress
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