The study "supports the contention that the failing human heart retains the capacity for recovery," they said.
If overexpression has been functionally demonstrated in ventricular myocytes from failing human hearts.
Conclusions: NAGE gene and protein expression were selectively activated in left ventricular myocytes from end-stage failing human hearts.
However, in failing human hearts NAGE gene expression was selectively activated in cardiac myocytes, but not endothelial cells.
While it is known that ADM is increased in failing human ventricles, the expression of ADM in human ventricular allografts remains unknown.
Tissue-engineered regeneration of a failing human heart remains a major challenge, while cardiovascular disease continues to take more lives than all cancers combined.
The replacement or augmentation of failing human organs with artificial devices and systems has been an important element in health care for several decades.
This study tested the hypothesis that NAGE is present in the human heart and that NAGE expression is increased in the failing human heart.
In general, the failing human heart is characterized by a selective reduction in β1-adrenoceptors (β1-ARs) without change in β2-AR density.
In accordance, β2-subunit mRNA and protein are up-regulated in failing human myocardium.
Liesmaa and collaborators identified increased expression of B1R in endothelium of failing human hearts.
