2019
DOI: 10.1016/j.yjmcc.2019.01.030
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Dedicator of cytokinesis 2 silencing therapy inhibits neointima formation and improves blood flow in rat vein grafts

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Cited by 7 publications
(6 citation statements)
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“…Conversely, DOCK2 knockout was shown to increase VSMC marker protein expression, supporting an argument for the requirement of low level DOCK2 expression in VSMCs to maintain contractile protein homeostasis [74]. A further study has implicated a role for DOCK2 in neointima formation, which is the generation of scar tissue in the blood vessel lumen after vein graft [75]. This was identified when unusually high levels of DOCK2 expression were detected in vein grafts of male Sprague-Dawley rats that underwent jugular vein-carotid artery bypass grafting [75].…”
Section: Dock2mentioning
confidence: 89%
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“…Conversely, DOCK2 knockout was shown to increase VSMC marker protein expression, supporting an argument for the requirement of low level DOCK2 expression in VSMCs to maintain contractile protein homeostasis [74]. A further study has implicated a role for DOCK2 in neointima formation, which is the generation of scar tissue in the blood vessel lumen after vein graft [75]. This was identified when unusually high levels of DOCK2 expression were detected in vein grafts of male Sprague-Dawley rats that underwent jugular vein-carotid artery bypass grafting [75].…”
Section: Dock2mentioning
confidence: 89%
“…A further study has implicated a role for DOCK2 in neointima formation, which is the generation of scar tissue in the blood vessel lumen after vein graft [75]. This was identified when unusually high levels of DOCK2 expression were detected in vein grafts of male Sprague-Dawley rats that underwent jugular vein-carotid artery bypass grafting [75]. Adding to existing knowledge of the role of DOCK2 in VSMC differentiation, DOCK2 knockdown was noted to inhibit rat VSMC migration and proliferation, whereas over-expression significantly increased these processes [75].…”
Section: Dock2mentioning
confidence: 99%
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“…It can inhibit the protein in the small intestine to transport cholesterol, thereby inhibiting the function of intestinal absorption of cholesterol, regulating plasma free cholesterol level, and reducing cholesterol storage level in the liver. This product can be used in combination with atorvastatin calcium to reduce LDL-C level [11] . While controlling a high-fat diet, it can be used independently to regulate blood lipids or in combination with HMG-CoA reductase inhibitors (statins) to treat hypercholesterolemia caused by various factors, which can significantly reduce plasma LDL-C, TC and Apolipoprotein B (ApoB) levels.…”
Section: Clinical Datamentioning
confidence: 99%