Cardiovascular Pathology 2022
DOI: 10.1016/b978-0-12-822224-9.00006-2
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Vascular Pathobiology: Atherosclerosis and Large Vessel Disease

Quinn A. Bonafiglia,
Michelle Bendeck,
Avrum I. Gotlieb
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Cited by 5 publications
(4 citation statements)
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“…Pathophysiology: Hereditary and acquired abnormalities that lead to the weakening and disruption of an elastic layer separating the vessels in the media and odontia, where the wall is inherently thinner and the turbulence of the bloodstream more likely to cause herniation and outflow of the vessel wall [6][7][8]. Causes of this condition include inheritance, atherosclerosis and hypertension, infections, malignancies, cigarette and alcohol abuse and substance abuse, and vascular disorders elsewhere in the body (such as the Romeo Roberto document, Coarcta Sion Aorta, etc.)…”
Section:  Aortic Infection After Aortic Surgerymentioning
confidence: 99%
“…Pathophysiology: Hereditary and acquired abnormalities that lead to the weakening and disruption of an elastic layer separating the vessels in the media and odontia, where the wall is inherently thinner and the turbulence of the bloodstream more likely to cause herniation and outflow of the vessel wall [6][7][8]. Causes of this condition include inheritance, atherosclerosis and hypertension, infections, malignancies, cigarette and alcohol abuse and substance abuse, and vascular disorders elsewhere in the body (such as the Romeo Roberto document, Coarcta Sion Aorta, etc.)…”
Section:  Aortic Infection After Aortic Surgerymentioning
confidence: 99%
“…Studies have indicated that the neovessels primarily originate from a pre-existing vasa vasorum, which constitutes a microvasculature network responsible for supplying arterial walls [34,35]. Neovessels are commonly found in the fibrous cap as well as in the medial and lateral corners of plaques, but their presence at the base is infrequent [36]. The development of new pathological capillaries promotes macrophage infiltration, inflammation, and lipid deposition as well as intraplaque hemorrhages that contribute to a progressive increase in the instability of plaques [37].…”
Section: Vulnerable Plaquesmentioning
confidence: 99%
“…The relevance of somatic mutations in PAD progression lies in the potential to disrupt critical cellular processes involved in maintaining vascular health, promoting atherosclerotic plaque formation, altering the vascular tone, and remodeling and modulating angiogenesis [2]. Somatic mutations can affect genes involved in lipid Biomedicines 2023, 11, 2288 2 of 16 metabolism, extracellular matrix (ECM) remodeling, and endothelial cell (EC) function, thereby influencing plaque stability and arterial remodeling [4]. Additionally, mutations in genes regulating angiogenesis can impact the development of collateral vessels, which are essential compensatory mechanisms in PAD [5].…”
Section: Introductionmentioning
confidence: 99%
“…and modulating angiogenesis [2]. Somatic mutations can affect genes involved in lipid metabolism, extracellular matrix (ECM) remodeling, and endothelial cell (EC) function, thereby influencing plaque stability and arterial remodeling [4]. Additionally, mutations in genes regulating angiogenesis can impact the development of collateral vessels, which are essential compensatory mechanisms in PAD [5].…”
Section: Introductionmentioning
confidence: 99%