Whole-genome array from intense light-exposed wild-type or Per2<sup>-/-</sup> mice and myocardial ischemia in endothelial-specific PER2-deficient mice uncover a critical role for intense light in maintaining endothelial barrier function via light-enhanced HIF1A transcription.
This review addresses our current understanding of the connection between light-sensing pathways (PER2), and oxygen-sensing pathways (HIF1A), in the context of myocardial ischemia and lays the groundwork for future studies to take advantage of these two evolutionarily conserved pathways in the treatment of myocardial ischemia.
Ad-HIF-1α-Trip is able to improve angiogenesis and cardiac function, which may be a promising avenue for treatment of ischemic heart disease in the future.
Analysis of animal models suggests that by activation of these homeostatic mechanisms, HIF-1 plays a critical protective role in the pathophysiology of ischemic heart disease and pressure-overload heart failure.
The findings indicate not any significant association between collateral formation and polymorphic variants of HIF-1A and P582S substitution does not appear to influence the collateral formation in patients with myocardial ischemia.
Because hypoxia-inducible factor (HIF)-1alpha is a transcriptional activator of vascular endothelial growth factor (VEGF) and is critical for initiating angiogenic responses to hypoxia, we investigated the expression of HIF-1alpha and VEGF in specimens of human heart tissue to elucidate the molecular responses to myocardial ischemia in diabetic patients during unstable angina.