As the heart muscle
becomes thicker the chambers within the heart get smaller and so can hold a smaller volume of blood.
Cell biologists have been historically unable to induce heart muscle
cells to get past the point in development characteristic of newborns, even when they let them mature in dishes for a year.
But this ability of heart muscle
to regenerate is quickly lost in the following weeks as the animal ages and the cells are bathed in the oxygen-rich environment of the beating heart, causing damage to the cells.
Within a couple of days, the micro tissues resembled heart muscle
both structurally and functionally.
Less common causes of HF include faulty heart valves, damage to the heart muscle
(cardiomyopathy due to certain diseases, alcohol and substance abuse), inflammation of the heart muscle
(myocarditis, usually caused by a viral infection) and congenital heart defects.
Kuhn points out that research in the 1930s and 1940s suggested that cardiomyocyte division may continue after birth, and recent reports about myocardial regeneration in zebrafish and neonatal mice suggest that some young animals regenerate heart muscle
by using mechanisms of muscle cell division.
The GMT genes alone reduced the amount of scar tissue by half, and there were more heart muscle
cells in the animals that were treated with GMT.
In DCM, the heart muscle
wall becomes thin and floppy, and is described as being dilated or 'baggy'.
Mice treated with thymosin beta-4 for a week before a heart attack produced a small number of new heart muscle
cells, but mice given the drug only after a heart attack didn't.
After the aortic valve is replaced, the heart muscle
begins to shrink back to its normal size and shape.
By monitoring carbon 14, originally emitted from bomb tests during the Cold War nuclear era, they found that heart muscle
cells continue to divide throughout adulthood.
From embryonic stem cells extracted from mice, scientists at Duke University successfully grew heart muscle
cells known as cardiomyocytes.