@Article{ecn.2013.0335,
AUTHOR = {Fouad A. Zouein, Mazen Kurdi, George W. Booz},
TITLE = {LIF and the heart: Just Another Brick in the Wall?*},
JOURNAL = {European Cytokine Network},
VOLUME = {24},
YEAR = {2013},
NUMBER = {1},
PAGES = {11--19},
URL = {http://www.techscience.com/ECN/v24n1/65677},
ISSN = {1952-4005},
ABSTRACT = {Multiple studies have shown that the cytokine leukemia inhibitory factor (LIF) is protective of the
myocardium in the acute stress of ischemia-reperfusion. All three major intracellular signaling pathways that are
activated by LIF in cardiac myocytes have been linked to actions that protect against oxidative stress and cell death,
either at the level of the mitochondrion or via nuclear transcription. In addition, LIF has been shown to contribute
to post-myocardial infarction cardiac repair and regeneration, by stimulating the homing of bone marrow-derived
cardiac progenitors to the injured myocardium, the differentiation of resident cardiac stem cells into endothelial
cells, and neovascularization. Whether LIF offers protection to the heart under chronic stress such as hypertensioninduced
cardiac remodeling and heart failure is not known. However, mice with cardiac myocyte restricted knockout
of STAT3, a principal transcription factor activated by LIF, develop heart failure with age, and cardiac STAT3 levels
are reported to be decreased in heart failure patients. In addition, endogenously produced LIF has been implicated
in the cholinergic transdiffrentiation that may serve to attenuate sympathetic overdrive in heart failure and in
the peri-infarct region of the heart after myocardial infarction. Surprisingly, therapeutic strategies to exploit the
beneficial actions of LIF on the injured myocardium have received scant attention. Nor is it established whether
the purported so-called adverse effects of LIF observed in isolated cardiac myocytes have physiological relevance
in vivo. Here we present an overview of the actions of LIF in the heart with the goal of stimulating further research
into the translational potential of this pleiotropic cytokine.},
DOI = {10.1684/ecn.2013.0335}
}