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Placental Growth Factor Regulates Cardiac Inflammation Through the Tissue Inhibitor of Metalloproteinases-3/Tumor Necrosis Factor-α–Converting Enzyme Axis
Author(s) -
Daniela Carnevale,
Giuseppe Cifelli,
Giada Mascio,
Michele Madonna,
Mauro Sbroggió,
Cinzia Perrino,
Maria Grazia Persico,
Giacomo Frati,
Giuseppe Lembo
Publication year - 2011
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.111.050500
Subject(s) - pressure overload , tumor necrosis factor alpha , medicine , endocrinology , angiogenesis , placental growth factor , inflammation , vascular endothelial growth factor , growth factor , matrix metalloproteinase , cancer research , heart failure , receptor , cardiac hypertrophy , vegf receptors
Heart failure is one of the leading causes of mortality and is primarily the final stage of several overload cardiomyopathies, preceded by an early adaptive hypertrophic response and characterized by coordinated cardiomyocyte growth, angiogenesis, and inflammation. Therefore, growth factors and cytokines have to be critically regulated during cardiac response to transverse aortic constriction. Interestingly, the dual properties of placental growth factor as an angiogenic factor and cytokine make it a candidate to participate in cardiac remodeling in response to hemodynamic overload.

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