Advancing age increases the size and severity of spontaneous atheromas in mouse models of atherosclerosis.
Advancing age increases the size and severity of spontaneous atheromas in mouse models of atherosclerosis.
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DOI:
10.1007/s11357-023-00776-8
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发表时间:
2023-06
期刊:
影响因子:
5.6
通讯作者:
Lesniewski, Lisa A.
中科院分区:
文献类型:
--
作者:
Gogulamudi, Venkateswara R.;Durrant, Jessica R.;Adeyemo, Adelola O.;Ho, Huynh Mi;Walker, Ashley E.;Lesniewski, Lisa A.
Using multiple mouse models, we explored the impact of aging on the size and severity of atherosclerotic lesions. In young, middle-aged and old apolipoprotein E knockout mice (ApoE−/−) fed an atherogenic diet (AD) for 3–8 weeks, plaque/atheroma formation in the descending aorta and aortic root, and atheroma development in the carotid in response to partial carotid ligation (PCL) were assessed. Total and LDL cholesterol, and triglycerides were higher in old compared to both other age groups, regardless of AD duration. Aortic plaque burden increased with AD duration in all ages. The size and plaque morphology grade of aortic root atheromas was higher with age; however, there was no effect of age on the size or severity of carotid atheromas after PCL. We additionally induced hyperlipidemia in young and old C57BL/6 mice by adeno-associated virus mediated upregulation of LDL receptor regulator, Pcsk9, and 5 weeks of AD. Despite lower cholesterol in old compared to young Pcsk9 mice, there was a greater size and severity of aortic root atheromas in old mice. However, like the ApoE−/− mice, there was no effect of age on size or severity of PCL-induced carotid artery atheromas in Pcsk9 mice. Together, these results suggest that aging increases the size and severity of spontaneous aortic atheromas. The online version contains supplementary material available at 10.1007/s11357-023-00776-8.
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影响因子:
37.8
作者:
Go AS;Mozaffarian D;Roger VL;Benjamin EJ;Berry JD;Blaha MJ;Dai S;Ford ES;Fox CS;Franco S;Fullerton HJ;Gillespie C;Hailpern SM;Heit JA;Howard VJ;Huffman MD;Judd SE;Kissela BM;Kittner SJ;Lackland DT;Lichtman JH;Lisabeth LD;Mackey RH;Magid DJ;Marcus GM;Marelli A;Matchar DB;McGuire DK;Mohler ER 3rd;Moy CS;Mussolino ME;Neumar RW;Nichol G;Pandey DK;Paynter NP;Reeves MJ;Sorlie PD;Stein J;Towfighi A;Turan TN;Virani SS;Wong ND;Woo D;Turner MB;American Heart Association Statistics Committee and Stroke Statistics Subcommittee
通讯作者:
American Heart Association Statistics Committee and Stroke Statistics Subcommittee
影响因子:
8.3
作者:
Meschia JF;Bushnell C;Boden-Albala B;Braun LT;Bravata DM;Chaturvedi S;Creager MA;Eckel RH;Elkind MS;Fornage M;Goldstein LB;Greenberg SM;Horvath SE;Iadecola C;Jauch EC;Moore WS;Wilson JA;American Heart Association Stroke Council;Council on Cardiovascular and Stroke Nursing;Council on Clinical Cardiology;Council on Functional Genomics and Translational Biology;Council on Hypertension
通讯作者:
Council on Hypertension
影响因子:
7.8
作者:
Lesniewski LA;Seals DR;Walker AE;Henson GD;Blimline MW;Trott DW;Bosshardt GC;LaRocca TJ;Lawson BR;Zigler MC;Donato AJ
通讯作者:
Donato AJ
DOI:
10.1161/hypertensionaha.110.165365
发表时间:
2011-03
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
作者:
Padilla J;Simmons GH;Fadel PJ;Laughlin MH;Joyner MJ;Casey DP
通讯作者:
Casey DP
影响因子:
3.9
作者:
Lesniewski, Lisa A.;Zigler, Melanie L.;Durrant, Jessica R.;Nowlan, Molly J.;Folian, Brian J.;Donato, Anthony J.;Seal, Douglas R.
通讯作者:
Seal, Douglas R.