Endothelial aging

Brandes, Ralf P.; Fleming, Ingrid; Busse, Rudi

doi:10.1016/j.cardiores.2004.12.027

Cited by 542 publications

(478 citation statements)

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“…ROS induce export of nuclear TERT into the cytosol through activation of Src-family kinases. 134,135 Inhibition of nuclear TERT activity shortens telomere length, leading to decrease in the endothelial cell's life span, alteration in gene expression and change from phenotype of young cells to phenotype of old cells. 136 In addition, telomere shortening stimulates activation of p53, p21 and p16 proteins, which are triggers of cell senescence.…”

Section: Endothelial Cell Senescencementioning

confidence: 99%

Endothelial dysfunction and hypertension in aging

2012

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Hypertension is one of the common diseases in the elderly. The prevalence of hypertension markedly increases with advancing age. Both aging and hypertension have a critical role in cardiovascular and cerebrovascular complications. Although aging and hypertension, either independently or collectively, impair endothelial function, aging and hypertension may have similar cascades for the pathogenesis and development of endothelial dysfunction. Nitric oxide (NO) has an important role in regulation of vascular tone. Decrease in NO bioavailability by endothelial dysfunction would lead to elevation of blood pressure. An imbalance of reduced production of NO or increased production of reactive oxygen species, mainly superoxide, may promote endothelial dysfunction. One possible mechanism by which the prevalence of hypertension is increased in relation to aging may be advancing endothelial dysfunction associated with aging through an increase in oxidative stress. In addition, endothelial cell senescence is also involved in aging-related endothelial dysfunction. In this review, we focus on recent findings and interactions between endothelial function, oxidative stress and hypertension in aging.

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Section: Endothelial Cell Senescencementioning

confidence: 99%

Endothelial dysfunction and hypertension in aging

2012

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“…↑ ↓ Endothelial function ↓ NK activity ↑ Glial activation (Gomez et al 2007;Hazeldine et al 2012;Morgan et al 1999;Brandes et al 2005) (Tureyen et al 2007;Hatashita et al 1990;Cole et al 1993;Dawson et al 1996;Porritt et al 2010;Mariucci et al 2011) Infection / PAMP-induced systemic inflammation mouse male Infarct size ↑, BBB injury ↑, mortality ↑, vascular injury ↑, brain inflammation ↑, Inflammatory cells in the brain ↑ IL-1, RANTES (CCL5), MMP-9, neutrophils, (McColl et al 2007(McColl et al , 2008Denes et al 2011a;Denes et al 2010a;Muhammad et al 2011) Stress rat male Infarct size ↑, behavioral outcome ↓, endothelial function ↓, superoxide production ↑ TNFα, glucocorticoids (Balkaya et al 2011b;Caso et al 2009;Madrigal et al 2003;Sugo et al 2002;Caso et al 2006) …”

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The Immune System in Stroke: Clinical Challenges and Their Translation to Experimental Research

Smith

Lawrence

Rodriguez‐Grande

et al. 2013

J Neuroimmune Pharmacol

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Stroke represents an unresolved challenge for both developed and developing countries and has a huge socio-economic impact. Although considerable effort has been made to limit stroke incidence and improve outcome, strategies aimed at protecting injured neurons in the brain have all failed. This failure is likely to be due to both the incompleteness of modelling the disease and its causes in experimental research, and also the lack of understanding of how systemic mechanisms lead to an acute cerebrovascular event or contribute to outcome.Inflammation has been implicated in all forms of brain injury and it is now clear that immune mechanisms profoundly influence (and are responsible for the development of) risk and causation of stroke, and the outcome following the onset of cerebral ischemia. Until very recently, systemic inflammatory mechanisms, with respect to common comorbidities in stroke, have largely been ignored in experimental studies. The main aim is therefore to understand interactions between the immune system and brain injury in order to develop novel therapeutic approaches. Recent data from clinical and experimental research clearly show that systemic inflammatory diseases -such as atherosclerosis, obesity, diabetes or infectionsimilar to stress and advanced age, are associated with dysregulated immune responses which can profoundly contribute to cerebrovascular inflammation and injury in the central nervous system. In this review, we summarize recent advances in the field of inflammation and stroke, focusing on the challenges of translation between pre-clinical and clinical studies, and potential anti-inflammatory/immunomodulatory therapeutic approaches.

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“…Toutefois, la sénescence peut aussi être déclenchée indépendamment de la longueur des télomères, en présence de diverses sources de stress (oncogènes, rayons UV, irradiations, stress oxydant). On parle alors de sénescence induite prématurément par le stress concept général s'applique aussi au système vasculaire et aux cellules endothéliales [6,8]. Il n'existe toutefois aucune théorie capable d'expliquer les causes et les mécanismes de toutes les facettes du vieillissement.…”

Section: Vieillissement Cellulaire Ou Sénescence Cellulaireunclassified

“…La dysfonction endothéliale caractéristique du vieillissement vasculaire [6] se traduit par une baisse de la capacité vasodilatatrice de l'endothélium [31] et par un déséquilibre des facteurs endothéliaux Figure 1. Activation des cascades de signalisation de la sénescence par différents stimulus.…”

Section: Vieillissement Endothélial Dans Un Environnement Pro-oxydantunclassified

“…Le vieillissement, la sénescence et finalement la mort, résultent de l'inefficacité à maintenir l'homéostasie cellulaire et à réparer les dommages. Les cellules endothéliales sont très sensibles au stress oxydant et leur dysfonction est une caractéristique du vieillissement vasculaire [6]. Toutefois, en accord avec le principe d'hormesis, une exposition précoce des cellules endothéliales, durant leur phase de maturation, à de faibles concentrations de radicaux libres, devrait augmenter leur longévité vasculaire.…”

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