Placental growth factor as a protective paracrine effector in the heart.
In response to injury, the myocardium hypertrophies in an attempt to maintain or augment function, which is associated with ventricular remodeling and changes in capillary density. During the compensatory phase of the hypertrophic response, the myocardium maintains output and is characterized by a coordinated neo-angiogenic and fibrotic response that supports cardiomyocyte health and survival. Emerging evidence shows that paracrine-mediated cross talk between cardiac myocytes and nonmyocytes within the heart is critical for cardiac adaptation to stress, including the extent of hypertrophy and angiogenesis. This review discusses recent results indicating that placental growth factor (PGF; also called PlGF), a secreted factor within the vascular endothelial growth factor superfamily, is a pivotal mediator of adaptive cardiac hypertrophy and beneficial angiogenesis through its ability to coordinate the intercellular communication between different cell types in the heart.
Department of Pediatrics, Division of Molecular Cardiovascular Biology and the Howard Hughes Medical Institute, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Federica
F
Accornero
Jeffery D
JD
Molkentin
D000222:Adaptation, Physiological; D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018919:Neovascularization, Physiologic; D019899:Paracrine Communication; D000072483:Placenta Growth Factor; D011257:Pregnancy Proteins / Q000378:metabolism*; D015398:Signal Transduction; D020257:Ventricular Remodeling
C000608036:PGF protein, human; D011257:Pregnancy Proteins; D000072483:Placenta Growth Factor