Metabolic changes in the heart have been implicated in the increased incidence of myocardial infarction [ 2], with diabetic patients having decreased cardiac glucose metabolism and increased cardiac fatty acid metabolism [ 3- 6].
Currently, the role of glucose signaling independent of its energy-providing effects is largely unaddressed in the hypertrophic and failing heart, but has been implicated to play an important role in myocyte function and survival (Kolwicz et al, 2013).
Brn-3b and Brn-3a expression have previously been reported in cardiomyocytes, whereas p53 is undetectable in healthy adult hearts but has been implicated in different cardiac pathologies, including hypoxia and ischaemia/reperfusion (I/R) injury.
Although Rac1 has not been previously implicated in myocardial development, as Rac1 null mice die early in development before the heart is well formed, it has been implicated in adult cardiovascular pathologies.
Moreover, it has been suggested that lung function is more strongly associated with risk of fatal rather than nonfatal coronary heart disease (CHD) events and has been implicated in increased fatality following a cardiac event (10).
In particular, for coronary heart diseases, no particular food has been implicated as causal, but the evidence for a favourable role of the Mediterranean dietary pattern is convincing (Mente et al, 2009).
NPY activation of the Y5R has been implicated in heart function, primarily in promoting cardiac hypertrophy (thickening of the heart muscle) via MAP kinase signalling (Pellieux et al, 2000).
PKCε has been implicated in heart protection and ventricular hypertrophy.
Slit-Robo signalling has been implicated in heart tube assembly and lumen formation in Drosophila and zebrafish development, and in cardiac chamber formation, pericardial development, and cardiac neural crest migration and adhesion during murine heart development.
Nevertheless, the possible role of the MPTP opening in apoptotic cell death has been implicated in heart muscle cells in normal mice that have high levels of CypD as well as in neurons exposed to moderate calcium overload.
