Endothelial progenitor cells induce transplant arteriosclerosis via VEGFR-1/2 activity

Yang, Zhaohua; Wang, Can; Yang, Shouguo; Hong, Tao; Wang, Fangshun; Xia, Limin; Wang, Chunsheng

doi:10.1016/j.atherosclerosis.2014.11.014

Cited by 6 publications

(5 citation statements)

References 21 publications

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“…However, there seems to be a gradual increase in VEGF concentrations by worsening of atherosclerosis [10]; increased circulating levels of VEGF have been correlated with adverse prognosis in acute coronary syndromes [7]; an increasing number of studies reported a major contribution for VEGF to plaque development and progression, and to calcification processes [5][6][7]43,[47][48]. Finally, inhibitors of VEGF receptors can reduce arteriosclerosis induced by abdominal aorta transplantation in animals [49].…”

Section: Discussionmentioning

confidence: 99%

Does statin therapy reduce plasma VEGF levels in humans? A systematic review and meta-analysis of randomized controlled trials

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Does statin therapy reduce plasma VEGF levels in humans? A systematic review and meta-analysis of randomized controlled trials

et al. 2015

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“…Specifically, we show, 8 An important limitation of both of these studies is the non-specific effect of tyrosine kinase inhibition. In the present study, we employ a soluble VEGFR1 inhibitor which acts by way of specifically reducing the bioavailability of VEGF.…”

Section: Discussionmentioning

confidence: 80%

“…8 In addition, other studies have suggested an association between circulating EPCs and risk for frequency of EPCs among subjects with transplant arteriosclerosis they hypothesized that this circulating depletion was due to EPC migration and localization to affected areas in transplanted hearts. 36 Although the mouse heterotopic model of cardiac transplantation is a widely accepted system in which to study mechanisms of rejection, functional differences as compared to the human transplant model are recognized.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of vascular endothelial growth factor reduces cardiac allograft vasculopathy

Chatur

Wong

Carthy

et al. 2016

The Journal of Heart and Lung Transplantation

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“…EPCs can be classified in early endothelial progenitor cells (eEPCs) and late endothelial progenitor cells, or most commonly called endothelial colony forming cells (ECFCs; Fadini et al, 2012). The first subgroup (eEPCs) seems to act preferably in a paracrine way, secreting numerous angiogenic factors, like VEGF (Yang et al, 2015). On the other hand, ECFCs are highly proliferative and can promote angiogenesis in vitro and in vivo and are involved in wound healing (Fadini et al, 2012).…”

Section: Potential Therapeutic Targets For Ed In Bav Diseasementioning

confidence: 99%

Bicuspid Aortic Valve and Endothelial Dysfunction: Current Evidence and Potential Therapeutic Targets

2020

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Bicuspid aortic valve (BAV), the most frequent congenital heart malformation, is characterized by the presence of a two-leaflet aortic valve instead of a three-leaflet one. BAV disease progression is associated with valvular dysfunction (in the form of stenosis or regurgitation) and aortopathy, which can lead to aneurysm and aortic dissection. This morphological abnormality modifies valve dynamics and promotes eccentric blood flow, which gives rise to alterations of the flow pattern and wall shear stress (WSS) of the ascending aorta. Recently, evidence of endothelial dysfunction (ED) in BAV disease has emerged. Different studies have addressed a reduced endothelial functionality by analyzing various molecular biomarkers and cellular parameters in BAV patients. Some authors have found impaired functionality of circulating endothelial progenitors in these patients, associating it with valvular dysfunction and aortic dilation. Others focused on systemic endothelial function by measuring artery flow-mediated dilation (FMD), showing a reduced FMD in BAV individuals. Novel biomarkers like increased endothelial microparticles (EMP), which are related to ED, have also been discovered in BAV patients. Finally, latest studies indicate that in BAV, endothelial-to-mesenchymal transition (EndoMT) may also be de-regulated, which could be caused by genetic, hemodynamic alterations, or both. Different hypothesis about the pathology of ED in BAV are nowadays being debated. Some authors blamed this impaired functionality just on genetic abnormalities, which could lead to a pathological aorta. Nevertheless, thanks to the development of new and high-resolution imaging techniques like 4D flow MRI, hemodynamics has gained great attention. Based on latest studies, alterations in blood flow seem to cause proper modification of the endothelial cells (ECs) function and morphology. It also seems to be associated with aortic dilation and decreased vasodilators expression, like nitric oxide (NO). Although nowadays ED in BAV has been reported by many, it is not clear which its main cause may be. Comprehending the pathways that promote ED and its relevance in BAV could help further understand and maybe prevent the serious consequences of this disease. This review will discuss the ED present in BAV, focusing on the latest evidence, biomarkers for ED and potential therapeutic targets (Figure 1).

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Endothelial progenitor cells induce transplant arteriosclerosis via VEGFR-1/2 activity

Cited by 6 publications

References 21 publications

Does statin therapy reduce plasma VEGF levels in humans? A systematic review and meta-analysis of randomized controlled trials

Does statin therapy reduce plasma VEGF levels in humans? A systematic review and meta-analysis of randomized controlled trials

Inhibition of vascular endothelial growth factor reduces cardiac allograft vasculopathy

Bicuspid Aortic Valve and Endothelial Dysfunction: Current Evidence and Potential Therapeutic Targets

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