Atypical chemokine receptor 1 deficiency reduces atherogenesis in ApoE-knockout mice | Zendy

Wuzhou Wan | Zendy; Qian Liu | Zendy; Michail S. Lionakis | Zendy; Ana Paula M.P. Marino | Zendy; Stasia A. Anderson | Zendy; Muthulekha Swamydas | Zendy; Philip M. Murphy | Zendy

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Atypical chemokine receptor 1 deficiency reduces atherogenesis in ApoE-knockout mice

Author(s) -

Wuzhou Wan,

Qian Liu,

Michail S. Lionakis,

Ana Paula M.P. Marino,

Stasia A. Anderson,

Muthulekha Swamydas,

Philip M. Murphy

Publication year - 2015

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1093/cvr/cvv124

Subject(s) - apolipoprotein e , chemokine , inflammation , cxc chemokine receptors , knockout mouse , immunology , chemokine receptor , medicine , receptor , cc chemokine receptors , biology , disease

Atypical chemokine receptor 1 (Ackr1; previously known as the Duffy antigen receptor for chemokines or Darc) is thought to regulate acute inflammatory responses in part by scavenging inflammatory CC and CXC chemokines; however, evidence for a role in chronic inflammation has been lacking. Here we investigated the role of Ackr1 in chronic inflammation, in particular in the setting of atherogenesis, using the apolipoprotein E-deficient (ApoE(-/-)) mouse model.

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