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Role of endothelial cell-derived angptl2 in vascular inflammation leading to endothelial dysfunction and atherosclerosis progression.
Eiji Horio
1 ,
Tsuyoshi Kadomatsu ,
Keishi Miyata ,
Yasumichi Arai ,
Kentaro Hosokawa ,
Yasufumi Doi ,
Toshiharu Ninomiya ,
Haruki Horiguchi ,
Motoyoshi Endo ,
Mitsuhisa Tabata ,
Hirokazu Tazume ,
Zhe Tian ,
Otowa Takahashi ,
Kazutoyo Terada ,
Motohiro Takeya ,
Hiroyuki Hao ,
Nobuyoshi Hirose ,
Takashi Minami ,
Toshio Suda ,
Yutaka Kiyohara ,
Hisao Ogawa ,
Koichi Kaikita ,
Yuichi Oike
Apr 2014
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Abstract
Cardiovascular disease (CVD), the most common morbidity resulting from atherosclerosis, remains a frequent cause of death. Efforts to develop effective therapeutic strategies have focused on vascular inflammation as a critical pathology driving atherosclerosis progression. Nonetheless, molecular mechanisms underlying this activity remain unclear. Here, we ask whether angiopoietin-like protein 2 (Angptl2), a proinflammatory protein, contributes to vascular inflammation that promotes atherosclerosis progression.