Epsin-mediated degradation of IP3R1 fuels atherosclerosis

Epsin-mediated degradation of IP3R1 fuels atherosclerosis

Endothelial cell (EC) dysfunction and inflammation contribute to plaque destabilization in atherosclerosis, increasing the risk of thrombotic events. Here, the authors show that epsin promotes EC inflammation via a mechanism involving IP3R1 degradation, and that deletion of epsin in the endothelium...

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Autores principales: Yunzhou Dong, Yang Lee, Kui Cui, Ming He, Beibei Wang, Sudarshan Bhattacharjee, Bo Zhu, Tadayuki Yago, Kun Zhang, Lin Deng, Kunfu Ouyang, Aiyun Wen, Douglas B. Cowan, Kai Song, Lili Yu, Megan L. Brophy, Xiaolei Liu, Jill Wylie-Sears, Hao Wu, Scott Wong, Guanglin Cui, Yusuke Kawashima, Hiroyuki Matsumoto, Yoshio Kodera, Richard J. H. Wojcikiewicz, Sanjay Srivastava, Joyce Bischoff, Da-Zhi Wang, Klaus Ley, Hong Chen
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2020
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Acceso en línea:https://doaj.org/article/348ebe71d77b44b0a5e82d323a1c1b08
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Sumario:Endothelial cell (EC) dysfunction and inflammation contribute to plaque destabilization in atherosclerosis, increasing the risk of thrombotic events. Here, the authors show that epsin promotes EC inflammation via a mechanism involving IP3R1 degradation, and that deletion of epsin in the endothelium prevents EC dysfunctoin and atherosclerosis in mice.

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