Vasa Vasorum in Normal and Diseased Arteries

Mulligan-Kehoe, Mary Jo; Simons, Michael

doi:10.1161/circulationaha.113.007189

Cited by 159 publications

(136 citation statements)

References 128 publications

(171 reference statements)

Supporting

Mentioning

121

Contrasting

Unclassified

Order By: Relevance

“…In particular, macrophages contribute critically to atherogenesis, both by collecting in atheroma lesions where they transform into lipid-rich foam cells, and by accumulating rapidly in the adventitia, where they facilitate formation of vasa vasorum and plaque microvessels, key regulators of atheroma burden and stability. 68,69 As in other tissues, vascular macrophages are heterogeneous, comprising proinflammatory M1, profibrotic, proangiogenic M2, and other subtypes. M1 cells have been found to dominate in rupture-prone shoulder regions of atheroma, whereas M2 macrophages are more common in adventitia, in early lesions and after plaque regression.…”

Section: Vascular Wall Hematopoietic Progenitor Cellsmentioning

confidence: 99%

“…61,62 Another obvious conduit for VW-PC delivery to vascular lesions is via adventitial vasa vasorum that expand under pathological conditions, and extend into adjacent plaque by guest on May 13, 2018 http://circres.ahajournals.org/ Downloaded from as thin-walled and leaky microvessels because of deficient pericyte coverage. 69 It has been well demonstrated that development of atheroma and its complications are closely related to the density and structural integrity of vasa vasorum, dependent on the stage of disease. 69 As highlighted by the activation of locally resident macrophage progenitors, EPCs and MSCs during arterial ring assays, VW-PCs are likely to contribute centrally to vasa vasorum formation, both by direct differentiation into ECs and pericytes, and by paracrine proangiogenic signaling.…”

Section: Vw-pcs In Diseasementioning

confidence: 99%

See 1 more Smart Citation

Vascular Wall Progenitor Cells in Health and Disease

2015

View full text Add to dashboard Cite

The vasculature plays an indispensible role in organ development and maintenance of tissue homeostasis, such that disturbances to it impact greatly on developmental and postnatal health. Although cell turnover in healthy blood vessels is low, it increases considerably under pathological conditions. The principle sources for this phenomenon have long been considered to be the recruitment of cells from the peripheral circulation and the re-entry of mature cells in the vessel wall back into cell cycle. However, recent discoveries have also uncovered the presence of a range of multipotent and lineage-restricted progenitor cells in the mural layers of postnatal blood vessels, possessing high proliferative capacity and potential to generate endothelial, smooth muscle, hematopoietic or mesenchymal cell progeny. In particular, the tunica adventitia has emerged as a progenitor-rich compartment with niche-like characteristics that support and regulate vascular wall progenitor cells. Preliminary data indicate the involvement of some of these vascular wall progenitor cells in vascular disease states, adding weight to the notion that the adventitia is integral to vascular wall pathogenesis, and raising potential implications for clinical therapies. This review discusses the current body of evidence for the existence of vascular wall progenitor cell subpopulations from development to adulthood and addresses the gains made and significant challenges that lie ahead in trying to accurately delineate their identities, origins, regulatory pathways, and relevance to normal vascular structure and function, as well as disease.

show abstract

Section: Vascular Wall Hematopoietic Progenitor Cellsmentioning

confidence: 99%

Section: Vw-pcs In Diseasementioning

confidence: 99%

Vascular Wall Progenitor Cells in Health and Disease

2015

View full text Add to dashboard Cite

show abstract

“…VV invasion can be observed when the vessel wall exceeds a certain thickness, which in mammals is 0.5 mm or 29 lamellar units. 3 It is assumed that the VV serve as a conduit for nutrients and oxygen, which can not be supplied to the adventitial and outer medial layers of the larger vessels by diffusion angiogenesis in adventitia promotes growth of atherosclerotic plaque in apolipoprotein e-deficient mice. cholesterolemia, atherosclerotic plaque progression was accompanied by an increased number of adventitial VV.…”

Section: Article P 1323mentioning

confidence: 99%

Visualization of the Human Coronary Vasa Vasorum In Vivo

Tanaka

Sata

2015

Circ J

View full text Add to dashboard Cite

“…The high-risk, rupture-prone atherosclerotic plaque is associated with a thin, fi brous cap, necrotic core extent and "spotty" pattern of calcifi cation, as well as plaque size and paradoxical positive remodelling [1,2]. Intraplaque neovascularisation and adventitial vasa vasorum, causing perivascular infl ammation according the "out-side-in theory" [3,4], as well as being potentially responsible for intraplaque haemorrhage, represent further important features of vulnerable plaques.…”

Section: Introductionmentioning

confidence: 99%

A combined “in vivo” noninvasive evaluation of carotid plaques using ultrasonography and high-resolution magnetic resonance - new insight into plaque burden and vulnerability

Porretta

Bianda

Valentino

et al. 2016

Vasa

View full text Add to dashboard Cite

Summary:Background: Qualitative change in carotid plaques was prospectively evaluated by Gray Scale Median (GSM) analysis at repeated examinations "in vivo", in relation to quantitative change in carotid arterial geometry, as assessed by high-resolution magnetic resonance imaging (HR-MRI). Patients and methods: Duplex ultrasound with GSM analysis and HR-MRI at the carotid level were performed at baseline and 1-and 2-year follow up in 30 patients with < 70% carotid stenosis. Changes in GSM values (ΔGSM) were evaluated as the intra-individual difference between 2-year and baseline values. HR-MRI studies were evaluated for lumen area (LA), total vessel area (TVA), vessel wall area (VWA = TVA-LA) and normalized wall index (NWI = VWA/TVA). Results: ΔGSM value distribution was divided into quartiles. Predominantly echolucent plaques with ΔGSM value in the lowest quartile (ΔGSM ≤-8) showed a signifi cantly greater mean 2-year LA (28.62 ± 10.9 mm 2 vs. 17.88 ± 4.8 mm 2 , p = 0.04) and a greater mean 2-year TVA (83.64 ± 19.4 mm 2 vs. 63.26 ± 9.2 mm 2 , p = 0.02) than predominantly echogenic plaques with ΔGSM value in the highest quartile (ΔGSM ≥8). Conclusions: Increasing echolucency during the 2-year follow up was associated with a 2-year lower degree of stenosis and higher tendency toward lumen preservation. By corroborating that plaque vulnerability is highly independent of stenosis severity, our study provided a possible new combined "in vivo" noninvasive approach for the assessment of carotid plaque vulnerability.

show abstract

Vasa Vasorum in Normal and Diseased Arteries

Cited by 159 publications

References 128 publications

Vascular Wall Progenitor Cells in Health and Disease

Vascular Wall Progenitor Cells in Health and Disease

Visualization of the Human Coronary Vasa Vasorum In Vivo

A combined “in vivo” noninvasive evaluation of carotid plaques using ultrasonography and high-resolution magnetic resonance - new insight into plaque burden and vulnerability

Contact Info

Product

Resources

About