Thalidomide influences atherogenesis in aortas of ApoE−/−/LDLR−/− double knockout mice: a nano-CT study

Kampschulte, Marian; Gunkel, I; Stieger, Philipp; Sedding, Daniel; Brinkmann, A; Ritman, Erik L.; Krombach, Gabriele A.; Langheinrich, Alexander C.

doi:10.1007/s10554-014-0380-5

Cited by 16 publications

(9 citation statements)

References 19 publications

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“…In further findings, Gõssl et al demonstrated that VV are not connected by a plexus but rather are end arteries ( 25 ). Using ex vivo micro-CT scans, we could demonstrate that this pathological sprouting pattern can also be observed in VV of small animal models of atherosclerosis, namely, apolipoprotein E −/− (ApoE)/LDLR −/− mice, and can be prevented by an antiangiogenic therapeutic approach ( 26 , 27 ). Moreover, structural hierarchy in adventitial VV was also later demonstrated in vivo in diseased LDLR −/− ApoB 100/100 mice by using high-resolution confocal microscopy ( 28 ).…”

Section: Correlation Between Arterial Wall Neovascularization and Athmentioning

confidence: 99%

“…Moreover, these mice exert an extensive angiogenic activity in the adventitia and develop prominent adventitial and intimal plaque VV ( 19 , 100 ). Since these mice most closely mimicked atherosclerotic plaques in humans, we and others have used this model extensively during the last years to study VV formation in mice ( 26 , 27 , 101 ). It is commonly supported by cardiovascular pathologists trained in human and experimental pathology ( 102 , 103 ) that murine plaques most closely resemble human plaque morphology.…”

Section: Animal Models To Study Vv and Plaque Rupture In Atheroscleromentioning

confidence: 99%

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Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease

et al. 2018

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Plaque microvascularization and increased endothelial permeability are key players in the development of atherosclerosis, from the initial stages of plaque formation to the occurrence of acute cardiovascular events. First, endothelial dysfunction and increased permeability facilitate the entry of diverse inflammation-triggering molecules and particles such as low-density lipoproteins into the artery wall from the arterial lumen and vasa vasorum (VV). Recognition of entering particles by resident phagocytes in the vessel wall triggers a maladaptive inflammatory response that initiates the process of local plaque formation. The recruitment and accumulation of inflammatory cells and the subsequent release of several cytokines, especially from resident macrophages, stimulate the expansion of existing VV and the formation of new highly permeable microvessels. This, in turn, exacerbates the deposition of pro-inflammatory particles and results in the recruitment of even more inflammatory cells. The progressive accumulation of leukocytes in the intima, which trigger proliferation of smooth muscle cells in the media, results in vessel wall thickening and hypoxia, which further stimulates neoangiogenesis of VV. Ultimately, this highly inflammatory environment damages the fragile plaque microvasculature leading to intraplaque hemorrhage, plaque instability, and eventually, acute cardiovascular events. This review will focus on the pivotal roles of endothelial permeability, neoangiogenesis, and plaque microvascularization by VV during plaque initiation, progression, and rupture. Special emphasis will be given to the underlying molecular mechanisms and potential therapeutic strategies to selectively target these processes.

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Section: Correlation Between Arterial Wall Neovascularization and Athmentioning

confidence: 99%

Section: Animal Models To Study Vv and Plaque Rupture In Atheroscleromentioning

confidence: 99%

Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease

et al. 2018

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“…Treatment with thalidomide preserved VV spatial density by 45% in high-cholesterol, diet-fed atherosclerosic pigs and was only 1.3-fold higher than that of normal pigs when compared with the 2.4-fold increase in the untreated group [ 171 ]. Reduced adventitial VV neovascularization and plaque progression after thalidomide treatment were also seen in Apoe −/− /Ldlr −/− double knockout mice [ 172 ]. The anti-angiogenic effect of thalidomide in atherosclerosis was accompanied by the inhibition of VEGF expression.…”

Section: Anti- and Pro-angiogenic Therapies On Vasa Vasorummentioning

confidence: 99%

Vasa Vasorum in Atherosclerosis and Clinical Significance

Shi

2015

IJMS

119

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Atherosclerosis is a chronic inflammatory disease that leads to several acute cardiovascular complications with poor prognosis. For decades, the role of the adventitial vasa vasorum (VV) in the initiation and progression of atherosclerosis has received broad attention. The presence of VV neovascularization precedes the apparent symptoms of clinical atherosclerosis. VV also mediates inflammatory cell infiltration, intimal thickening, intraplaque hemorrhage, and subsequent atherothrombosis that results in stroke or myocardial infarction. Intraplaque neovessels originating from VV can be immature and hence susceptible to leakage, and are thus regarded as the leading cause of intraplaque hemorrhage. Evidence supports VV as a new surrogate target of atherosclerosis evaluation and treatment. This review provides an overview into the relationship between VV and atherosclerosis, including the anatomy and function of VV, the stimuli of VV neovascularization, and the available underlying mechanisms that lead to poor prognosis. We also summarize translational researches on VV imaging modalities and potential therapies that target VV neovascularization or its stimuli.

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“…An experimental animal study examined the long-term effect of thalidomide on adventitial VV neovascularization and plaque progression using nano-focused computed tomography (nano-CT) of descending aortas. [65] Proliferation and migration assays in human coronary artery endothelial cells (HCAEC) measured the number of viable cells after incubation with thalidomide in ApoE (-/-)/LDLR (-/-) (AL) mice (n = 5) and a control group. Thalidomide inhibited proliferation and migration of HCAEC dose-dependently and VV neovascularization decreased in number per cross section.…”

Section: Computed Tomography Componentmentioning

confidence: 99%

Cardiovascular imaging 2014 in the International Journal of Cardiovascular Imaging

Bezerra¹,

Costa²,

Reiber³

et al. 2015

Int J Cardiovasc Imaging

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Thalidomide influences atherogenesis in aortas of ApoE−/−/LDLR−/− double knockout mice: a nano-CT study

Cited by 16 publications

References 19 publications

Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease

Vasa Vasorum Angiogenesis: Key Player in the Initiation and Progression of Atherosclerosis and Potential Target for the Treatment of Cardiovascular Disease

Vasa Vasorum in Atherosclerosis and Clinical Significance

Cardiovascular imaging 2014 in the International Journal of Cardiovascular Imaging

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