Chemerin-9 Attenuates Experimental Abdominal Aortic Aneurysm Formation in ApoE(-/-) Mice.
Chemerin-9 Attenuates Experimental Abdominal Aortic Aneurysm Formation in ApoE(-/-) Mice.
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DOI：
10.1155/2021/6629204
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发表时间：
2021
影响因子：
--
通讯作者：
Wu X
中科院分区：
文献类型：
--
作者：
Chen S;Han C;Bian S;Chen J;Feng X;Li G;Wu X
慢性炎症在腹主动脉瘤（AAA）的发病机制中起着重要作用，AAA是一种进行性节段性腹主动脉扩张。Chemerin是一种多功能脂肪细胞因子，主要在肝脏和脂肪组织中产生。趋化素和趋化因子样受体1（CMKLR1）的组合已被证明可促进动脉粥样硬化、关节炎疾病和克罗恩病的进展。然而，chemerin-9作为chemerin的类似物通过结合CMKLR 1发挥抗炎作用。在这里，我们首先证明，AAA表现出更高水平的chemerin和CMKLR1的表达与正常主动脉组织相比。因此，我们假设chemerin/CMKLR1轴可能参与AAA进展。此外，我们发现，chemerin-9治疗显着抑制炎症细胞浸润，新血管形成和基质金属蛋白酶（MMP）的表达，同时增加弹性纤维和平滑肌细胞（SMC）在血管紧张素II诱导的腹主动脉瘤在ApoE −/−小鼠。这表明chemerin-9可以抑制AAA形成。总的来说，我们的研究结果表明AAA进展的潜在机制，并表明chemerin-9可以用于治疗。
Chronic inflammation plays an essential role in the pathogenesis of abdominal aortic aneurysm (AAA), a progressive segmental abdominal aortic dilation. Chemerin, a multifunctional adipocytokine, is mainly generated in the liver and adipose tissue. The combination of chemerin and chemokine-like receptor 1 (CMKLR1) has been demonstrated to promote the progression of atherosclerosis, arthritis diseases, and Crohn's disease. However, chemerin-9 acts as an analog of chemerin to exert an anti-inflammatory effect by binding to CMKLR1. Here, we first demonstrated that AAA exhibited higher levels of chemerin and CMKLR1 expression compared with the normal aortic tissues. Hence, we hypothesized that the chemerin/CMKLR1 axis might be involved in AAA progression. Moreover, we found that chemerin-9 treatment markedly suppressed inflammatory cell infiltration, neovascularization, and matrix metalloproteinase (MMP) expression, while increasing the elastic fibers and smooth muscle cells (SMCs) in Ang II-induced AAA in ApoE−/− mice. This demonstrated that chemerin-9 could inhibit AAA formation. Collectively, our findings indicate a potential mechanism underlying AAA progression and suggest that chemerin-9 can be used therapeutically.
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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：
1.1
作者：
Eagleton, Matthew J.
通讯作者：
Eagleton, Matthew J.
DOI：
10.4103/1319-2442.275482
发表时间：
2019-11-01
影响因子：
0.5
作者：
El-Khashab, Sahier Omar;Gamil, Mona;Hamed, Soha Talat
通讯作者：
Hamed, Soha Talat
影响因子：
15.9
作者：
Longo, GM;Xiong, WF;Baxter, BT
通讯作者：
Baxter, BT
影响因子：
2
作者：
Lei, ZeLin;Lu, YaQin;Yu, Qin
通讯作者：
Yu, Qin