Fouad A Zouein

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Approximately half of heart failure patients have a normal ejection fraction, a condition designated as heart failure with preserved ejection fraction (HFpEF). This heart failure subtype disproportionately affects women and the elderly and is commonly associated with other cardiovascular comorbidities, such as hypertension and diabetes. HFpEF is increasing(More)
Microarrays do not yield direct evidence for functional connections between genes. However, transcription factors (TFs) and their binding sites (TFBSs) in promoters are important for inducing and coordinating changes in RNA levels, and thus represent the first layer of functional interaction. Similar to genes, TFs act only in context, which is why a(More)
A substantial body of evidence has shown that signal transducer and activator of transcription 3 (STAT3) has an important role in the heart in protecting the myocardium from ischemia and oxidative stress. These actions are attributed to STAT3 functioning as a transcription factor in upregulating cardioprotective genes. Loss of STAT3 has been implicated as(More)
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(More)
The four Janus kinases (JAKs) comprise a family of intracellular, nonreceptor tyrosine kinases that first gained attention as signaling mediators of the type I and type II cytokine receptors. Subsequently, the JAKs were found to be involved in signaling downstream of the insulin receptor, a number of receptor tyrosine kinases, and certain G-protein coupled(More)
The transcription factor, signal transducer and activator of transcription 3 (STAT3), has been implicated in protecting the heart from acute ischemic injury under both basal conditions and as a crucial component of pre- and post-conditioning protocols. A number of anti-oxidant and antiapoptotic genes are upregulated by STAT3 via canonical means involving(More)
Osteopontin is robustly upregulated following myocardial infarction (MI), which suggests that it has an important role in post-MI remodeling of the left ventricle (LV). Osteopontin deletion results in increased LV dilation and worsened cardiac function. Thus, osteopontin exerts protective effects post-MI, but the mechanisms have yet to be defined. Matrix(More)
Despite dramatic improvements in short-term mortality rates following myocardial infarction (MI), long-term survival for MI patients who progress to heart failure remains poor. MI occurs when the left ventricle (LV) is deprived of oxygen for a sufficient period of time to induce irreversible necrosis of the myocardium. The LV response to MI involves(More)
STAT3 is involved in protection of the heart provided by ischemic preconditioning. However, the role of this transcription factor in the heart in chronic stresses such as hypertension has not been defined. We assessed whether STAT3 is important in hypertension-induced cardiac remodeling using mice with reduced STAT3 activity due to a S727A mutation (SA/SA).(More)
Hearts of mice with reduction of function mutation in STAT3 (SA/SA) develop fibrotic collagen foci and reduced systolic function with hypertension. This model was used to determine if fractal dimension and image analysis can provide a quantitative description of myocardial fibrosis using routinely prepared trichome-stained material. Collagen was(More)