Disruption of the Apelin-APJ System Worsens Hypoxia-Induced Pulmonary Hypertension | Zendy

Suparna Chandra | Zendy; Hedi Razavi | Zendy; Jongmin Kim | Zendy; Rani Agrawal | Zendy; Ramendra K. Kundu | Zendy; Vinicio de Jesús Pérez | Zendy; Roham T. Zamanian | Zendy; Thomas Quertermous | Zendy; Hyung J. Chun | Zendy

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Disruption of the Apelin-APJ System Worsens Hypoxia-Induced Pulmonary Hypertension

Author(s) -

Suparna Chandra,

Hedi Razavi,

Jongmin Kim,

Rani Agrawal,

Ramendra K. Kundu,

Vinicio de Jesús Pérez,

Roham T. Zamanian,

Thomas Quertermous,

Hyung J. Chun

Publication year - 2011

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.110.219980

Subject(s) - apelin , enos , medicine , endocrinology , downregulation and upregulation , hypoxia (environmental) , klf2 , gene knockdown , nitric oxide synthase , nitric oxide , receptor , biology , chemistry , biochemistry , apoptosis , organic chemistry , oxygen , gene

The G-protein-coupled receptor APJ and its ligand apelin are highly expressed in the pulmonary vasculature, but their function in this vascular bed is unclear. We hypothesized that disruption of apelin signaling would lead to worsening of the vascular remodeling associated with pulmonary hypertension (PH).

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