1996
DOI: 10.1016/0021-9150(95)05727-7
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Modifications induced by atherogenic diet in the capacity of the arterial wall in rats to respond to surgical insult

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Cited by 17 publications
(19 citation statements)
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“…Smooth muscle cells are considered to be the main source of origin of osteogenic cells in calcified vascular lesions [16]. Other data indicate that the occurrence of ectopic medial calcifications is associated with adventitious cells [17]. Vessel and valve endothelial cells serve as a cellular barrier between the blood and the main tissue components, but participate in the endothelial-mesenchymal transition, playing a key role in tissue fibrosis and calcification [18].…”
Section: Discussionmentioning
confidence: 99%
“…Smooth muscle cells are considered to be the main source of origin of osteogenic cells in calcified vascular lesions [16]. Other data indicate that the occurrence of ectopic medial calcifications is associated with adventitious cells [17]. Vessel and valve endothelial cells serve as a cellular barrier between the blood and the main tissue components, but participate in the endothelial-mesenchymal transition, playing a key role in tissue fibrosis and calcification [18].…”
Section: Discussionmentioning
confidence: 99%
“…Indeed, surgical resection of the adventitia markedly reduces segmental medial artery calcification in a rat model of calcific vasculopathy (43). Such functional spatial relationships would help explain the circumferential pattern of medial artery calcification prevalent in diabetes.…”
Section: Figurementioning
confidence: 98%
“…14 and data not shown); thus, some diet-regulated metabolic parameter, potentially a phospholipid or oxidized sterol (6,8,51), synergizes with Msx2-Wnt signaling to drive medial calcification. Of note, surgical resection of the adventitia reduces segmental medial artery calcification (43); whether this arises from loss of adventitial pro-osteogenic paracrine signals, reductions in the vascular osteoprogenitor pool, or a combination of both is unknown. Cell surface markers that stratify vascular myofibroblast stages of development are currently lacking, but will be necessary to identify precisely how Msx2-Wnt signaling controls the fate of vascular mesenchymal cells.…”
Section: Figurementioning
confidence: 99%
“…High-fat diets upregulate aortic BMP2 expression (10). In addition to providing progenitors for medial disease processes (40,41,43), Msx2-expressing adventitial myofibroblasts produce an osteogenic milieu via induction of Wnt agonists and inhibition of the LRP5/6 antagonist, Dkk1. This causes nuclear localization and activation of β-catenin -an indispensable coregulator of osteoblast differentiation and mineralization (24); as reflected by TCF/LEF-dependent transcription, activation occurs in a subset of medial CVCs.…”
Section: Figure 11mentioning
confidence: 99%
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