Sex Differences in the LDL Receptor Knockout Mouse Model of Atherosclerosis.
作者信息
Mansukhani Neel A, Wang Zheng, Shively Vera P, Kelly Megan E, Vercammen Janet M, Kibbe Melina R
机构信息
Department of Surgery, Northwestern University, Chicago, IL.
Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC.
出版信息
Artery Res. 2017 Dec;20:8-11. doi: 10.1016/j.artres.2017.08.002. Epub 2017 Sep 21.
Abstract
摘要
相似文献
1
Sex Differences in the LDL Receptor Knockout Mouse Model of Atherosclerosis.动脉粥样硬化低密度脂蛋白受体基因敲除小鼠模型中的性别差异。
Artery Res. 2017 Dec;20:8-11. doi: 10.1016/j.artres.2017.08.002. Epub 2017 Sep 21.
2
Mixed testicular atrophy related to atherosclerosis: first lessons from the ApoE(-/-)/ LDL receptor(-/-) double knockout mouse model.与动脉粥样硬化相关的混合性睾丸萎缩：来自载脂蛋白E基因敲除/低密度脂蛋白受体基因敲除双敲除小鼠模型的初步经验教训
Int J Androl. 2012 Aug;35(4):562-71. doi: 10.1111/j.1365-2605.2011.01228.x. Epub 2011 Dec 13.
3
Myeloid cell-specific ATP-binding cassette transporter A1 deletion has minimal impact on atherogenesis in atherogenic diet-fed low-density lipoprotein receptor knockout mice.在喂食致动脉粥样硬化饮食的低密度脂蛋白受体敲除小鼠中，髓样细胞特异性ATP结合盒转运体A1缺失对动脉粥样硬化的影响极小。
Arterioscler Thromb Vasc Biol. 2014 Sep;34(9):1888-99. doi: 10.1161/ATVBAHA.114.303791. Epub 2014 May 15.
4
Atherosclerosis, vascular remodeling, and impairment of endothelium-dependent relaxation in genetically altered hyperlipidemic mice.基因改变的高脂血症小鼠的动脉粥样硬化、血管重塑及内皮依赖性舒张功能受损
Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2333-40. doi: 10.1161/01.atv.17.11.2333.
5
Extensive diet-induced atherosclerosis in scavenger receptor class B type 1-deficient mice is associated with substantial leukocytosis and elevated vascular cell adhesion molecule-1 expression in coronary artery endothelium.在缺乏1型清道夫受体B类的小鼠中，广泛的饮食诱导动脉粥样硬化与显著的白细胞增多以及冠状动脉内皮中血管细胞黏附分子-1表达升高有关。
Front Physiol. 2023 Jan 12;13:1023397. doi: 10.3389/fphys.2022.1023397. eCollection 2022.
6
The role of an experimental model of atherosclerosis: apoE-knockout mice in developing new drugs against atherogenesis.载脂蛋白 E 基因敲除小鼠在动脉粥样硬化发病机制新药研发中的作用。
Curr Pharm Biotechnol. 2012 Oct;13(13):2435-9.
7
Toll-like receptor 4 deficiency decreases atherosclerosis but does not protect against inflammation in obese low-density lipoprotein receptor-deficient mice.Toll 样受体 4 缺陷可减少动脉粥样硬化，但不能防止肥胖型低密度脂蛋白受体缺陷小鼠的炎症反应。
Arterioscler Thromb Vasc Biol. 2012 Jul;32(7):1596-604. doi: 10.1161/ATVBAHA.112.249847. Epub 2012 May 10.
8
Atherosclerosis, inflammation and lipoprotein glomerulopathy in kidneys of apoE-/-/LDL-/- double knockout mice.载脂蛋白 E 基因敲除/低密度脂蛋白受体基因敲除双基因敲除小鼠肾脏中的动脉粥样硬化、炎症和脂蛋白肾小球病。
BMC Nephrol. 2010 Aug 20;11:18. doi: 10.1186/1471-2369-11-18.
9
Inflammatory Cell-Derived MYDGF Attenuates Endothelial LDL Transcytosis to Protect Against Atherogenesis.炎性细胞衍生的 MYDGF 减弱内皮细胞 LDL 转胞吞作用，从而防止动脉粥样硬化形成。
Arterioscler Thromb Vasc Biol. 2023 Nov;43(11):e443-e467. doi: 10.1161/ATVBAHA.123.319905. Epub 2023 Sep 28.
10
Human paraoxonase-1 overexpression inhibits atherosclerosis in a mouse model of metabolic syndrome.人对氧磷酶-1过表达可抑制代谢综合征小鼠模型中的动脉粥样硬化。
Arterioscler Thromb Vasc Biol. 2006 Jul;26(7):1545-50. doi: 10.1161/01.ATV.0000222924.62641.aa. Epub 2006 Apr 20.
引用本文的文献
1
Current status and challenges of multi-omics research using animal models of atherosclerosis.使用动脉粥样硬化动物模型进行多组学研究的现状与挑战
J Mol Cell Cardiol Plus. 2025 Jul 10;13:100476. doi: 10.1016/j.jmccpl.2025.100476. eCollection 2025 Sep.
2
FFAR4 Deficiency Increases Necrotic Cores in Advanced Lesions of ApoE Mice-Brief Report.FFAR4基因缺陷增加载脂蛋白E基因敲除小鼠晚期病变中的坏死核心——简要报告
Arterioscler Thromb Vasc Biol. 2025 May;45(5):675-682. doi: 10.1161/ATVBAHA.124.322371. Epub 2025 Mar 6.
3
Thermoneutral-housed rats demonstrate impaired perivascular adipose tissue and vascular crosstalk.生活在热中性环境中的大鼠表现出血管周围脂肪组织和血管间相互作用受损。
J Hypertens. 2025 May 1;43(5):752-767. doi: 10.1097/HJH.0000000000003948. Epub 2025 Feb 7.
4
Endothelial KLF11 is a novel protector against diabetic atherosclerosis.内皮细胞 KLF11 是一种新型的糖尿病动脉粥样硬化保护因子。
Cardiovasc Diabetol. 2024 Oct 26;23(1):381. doi: 10.1186/s12933-024-02473-y.
5
GPX4 overexpression does not alter atherosclerotic plaque development in ApoE knock-out mice.谷胱甘肽过氧化物酶4（GPX4）的过表达不会改变载脂蛋白E基因敲除小鼠动脉粥样硬化斑块的发展。
Vasc Biol. 2024 Jun 3;6(1). doi: 10.1530/VB-23-0020. Print 2024 Jan 1.
6
Characterization of Atherosclerotic Mice Reveals a Sex-Dependent Susceptibility to Plaque Calcification but No Major Changes in the Lymphatics in the Arterial Wall.动脉粥样硬化小鼠的特征分析显示斑块钙化存在性别依赖性易感性，但动脉壁内淋巴管无明显变化。
Int J Mol Sci. 2024 Apr 5;25(7):4046. doi: 10.3390/ijms25074046.
7
CETP Expression in Bone-Marrow-Derived Cells Reduces the Inflammatory Features of Atherosclerosis in Hypercholesterolemic Mice.载脂蛋白 CETP 在骨髓源性细胞中的表达可降低高胆固醇血症小鼠动脉粥样硬化的炎症特征。
Biomolecules. 2023 Oct 22;13(10):1556. doi: 10.3390/biom13101556.
8
Neutrophil-specific STAT4 deficiency attenuates atherosclerotic burden and improves plaque stability via reduction in neutrophil activation and recruitment into aortas of mice.中性粒细胞特异性 STAT4 缺陷通过减少中性粒细胞活化和向小鼠主动脉的募集，减轻动脉粥样硬化负担并改善斑块稳定性。
Front Cardiovasc Med. 2023 Jun 16;10:1175673. doi: 10.3389/fcvm.2023.1175673. eCollection 2023.
9
Carbon Nanodots Attenuate Lipid Peroxidation in the LDL Receptor Knockout Mouse Brain.碳纳米点减轻低密度脂蛋白受体敲除小鼠大脑中的脂质过氧化
Antioxidants (Basel). 2023 May 11;12(5):1081. doi: 10.3390/antiox12051081.
10
DIAPH1 mediates progression of atherosclerosis and regulates hepatic lipid metabolism in mice.DIAPH1 介导动脉粥样硬化的进展并调节小鼠的肝脏脂质代谢。
Commun Biol. 2023 Mar 17;6(1):280. doi: 10.1038/s42003-023-04643-2.
本文引用的文献
1
Sex bias exists in basic science and translational surgical research.基础科学和转化性外科研究中存在性别偏见。
Surgery. 2014 Sep;156(3):508-16. doi: 10.1016/j.surg.2014.07.001.
2
Hyperlipidemia and atherosclerotic lesion development in Ldlr-deficient mice on a long-term high-fat diet.长期高脂饮食的 LDLR 缺陷型小鼠的高血脂症和动脉粥样硬化病变发展。
PLoS One. 2012;7(4):e35835. doi: 10.1371/journal.pone.0035835. Epub 2012 Apr 25.
3
Sex bias in neuroscience and biomedical research.神经科学和生物医学研究中的性别偏见。
Neurosci Biobehav Rev. 2011 Jan;35(3):565-72. doi: 10.1016/j.neubiorev.2010.07.002. Epub 2010 Jul 8.
4
Quantitative assay for mouse atherosclerosis in the aortic root.主动脉根部小鼠动脉粥样硬化的定量测定。
Methods Mol Med. 2006;129:83-95. doi: 10.1385/1-59745-213-0:83.
5
Induction of atherosclerosis by low-fat, semisynthetic diets in LDL receptor-deficient C57BL/6J and FVB/NJ mice: comparison of lesions of the aortic root, brachiocephalic artery, and whole aorta (en face measurement).低脂半合成饮食诱导低密度脂蛋白受体缺陷的C57BL/6J和FVB/NJ小鼠动脉粥样硬化：主动脉根部、头臂动脉和整个主动脉病变的比较（正面测量）
Arterioscler Thromb Vasc Biol. 2003 Oct 1;23(10):1907-13. doi: 10.1161/01.ATV.0000090126.34881.B1. Epub 2003 Aug 7.
6
Quantitation of atherosclerosis in murine models: correlation between lesions in the aortic origin and in the entire aorta, and differences in the extent of lesions between sexes in LDL receptor-deficient and apolipoprotein E-deficient mice.小鼠模型中动脉粥样硬化的定量分析：主动脉起始处与整个主动脉病变之间的相关性，以及低密度脂蛋白受体缺陷型和载脂蛋白E缺陷型小鼠两性之间病变程度的差异。
J Lipid Res. 1995 Nov;36(11):2320-8.
7
Hypercholesterolemia in low density lipoprotein receptor knockout mice and its reversal by adenovirus-mediated gene delivery.低密度脂蛋白受体基因敲除小鼠的高胆固醇血症及其通过腺病毒介导的基因递送的逆转。
J Clin Invest. 1993 Aug;92(2):883-93. doi: 10.1172/JCI116663.
8
Massive xanthomatosis and atherosclerosis in cholesterol-fed low density lipoprotein receptor-negative mice.胆固醇喂养的低密度脂蛋白受体阴性小鼠中的大量黄瘤病和动脉粥样硬化
J Clin Invest. 1994 May;93(5):1885-93. doi: 10.1172/JCI117179.
Zotero 插件