Circulating Endothelial Progenitor Cells in Cardiovascular Outcomes

Werner, Naomi; Kosiol, Sonja; Schiegle, T.

doi:10.1016/j.jvs.2005.12.021

Cited by 134 publications

(199 citation statements)

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“…Circulating angiogenic cells, such as endothelial progenitor cells, participate in the maintenance of the endothelium by acting as a cellular reservoir for the replacement of dysfunctional endothelial cells [27], or by releasing angiogenic growth factors [28]. The number of endothelial progenitor cells is a surrogate marker of vascular function, and low endothelial progenitor cell counts are associated with higher cardiovascular risk [26,29,30].…”

Section: Impairments In the Cerebrovascular System In Dementiamentioning

confidence: 99%

Primary Cerebral Blood Flow Deficiency and Alzheimer's Disease: Shadows and Lights

Mazza

Marano

Traversi

et al. 2011

JAD

107

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Alzheimer's disease (AD) is a degenerative disorder characterized by a decreased regional cerebral blood flow (CBF). It is most likely that a reduction in CBF could displace a pathway leading to AD genesis, in so far neuron death explains a sustained reduction in the supply of oxygen, glucose, and nutrients. Nevertheless, the concept of secondary CBF deficiency cannot explain the critical stages of early memory loss while, on the other hand, the picture of progressive ischemia due to primary CBF decline sheds light on the course of AD in a most persuasive manner. The concept of primary CBF deficiency is even more strengthened by the lack of correlation between degree of dementia and amount of CBF. Vascular abnormalities, frequently observed to co-occur with AD, might play a critical role in the initiation and aggravation of AD pathology given that the elimination of amyloid-β (Aβ) through a vascular route is an important brain Aβ clearance mechanism and its failure leads to formation of vascular amyloidosis and dense-core plaques. The goal of this review is to provide scientists comprehensive knowledge of the state-of the art influence vascular damage and reduced perfusion have on the final development of AD and to hopefully stimulate more research in this area of neuroscience.

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Section: Impairments In the Cerebrovascular System In Dementiamentioning

confidence: 99%

Primary Cerebral Blood Flow Deficiency and Alzheimer's Disease: Shadows and Lights

Mazza

Marano

Traversi

et al. 2011

JAD

107

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“…The implication of this finding is that the recruitment of EPC may thus be impaired in patients with impaired NO bioavailability. Indeed, several studies have provided data for a reduced number and perturbed functioning of circulating EPC in patients with cardiovascular risk factors, such as atherosclerotic disease,30 type 2 diabetes31 and coronary artery disease 32 33…”

Section: Endothelial Integrity: a Balance Between Injury And Repairmentioning

confidence: 99%

Inflammation, vascular injury and repair in rheumatoid arthritis

Zonneveld

Boer

Veer

et al. 2009

Annals of the Rheumatic Diseases

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The systemic pro-inflammatory state present in patients with rheumatoid arthritis (RA) accelerates the progression of atherosclerosis through chronic endothelial activation. Uncoupling of endothelial nitric oxide synthase plays a central role in the amplification of oxidative signalling pathways that chronically activate and, ultimately, injure the endothelium. Recent studies indicate that the resultant loss of endothelial integrity in patients with RA may also involve defects in the vascular regenerative potential provided by circulating endothelial progenitor cells (EPC). This is most likely the consequence of endothelial cell dysfunction in the bone marrow stroma, which hampers the mobilisation of these EPC to the circulation. In addition, mediators of systemic inflammation in RA can affect a second pathway of vascular regeneration. Under normal circumstances, myeloid CD14+ cells can adopt a pro-angiogenic phenotype that plays a key role in vascular remodelling and collateral formation. However, the chronic systemic inflammation observed in patients with RA may skew the differentiation of bone marrow and circulating CD14+ cells in such a way that these cells lose their capacity to support collateral formation, increasing the risk of cardiovascular disease. Taken together, in patients with RA, the impaired capacity of circulating cells to support vascular regeneration may comprise a novel pathway in the development of premature atherosclerosis.

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“…Although EPC levels have been considered as a surrogate marker of CV status in healthy subjects,11 12 different and even contradictory data about their role in RA patients have been reported. Recently, a novel T cell subset, the so-called angiogenic T cells (Tang),13 has been described that seems to cooperate with EPCs and enhance endothelial repair function, possibly through the secretion of proangiogenic cytokines.…”

Section: Introductionmentioning

confidence: 99%