Because they are interested in human heart failure, Lavine and his colleagues developed a method to progressively damage
mouse cardiac tissue in a way that mimicked heart failure.
Not exact matches
The researchers transplanted the
cardiac fibroblasts isolated from the region of calcification under the skin of healthy
mice and observed soft -
tissue calcification similar to that seen in the donor
mice.
In a study published online in Circulation Research late last year, Chaudhry and colleagues found that fetal cells in
mice migrated to the mother's heart, differentiated into functioning
cardiac cells, and accelerated repair to damaged heart
tissue.
«And when we examined the heart
tissue of the
mice that survived, we found that they had developed major regions of
cardiac muscle
tissue death.»
As the investigators note, the rapid age - related arterial stiffening and
cardiac arrhythmias that appear to be at cause for the majority of deaths in BubR1H / H
mice were not attenuated by ablating p16Ink4a - expressing senescent cells — but these
tissues had little burden of such cells, so this finding reinforces the conclusion that the multiple aging phenotypes arrested in these
mice when senescent cells were ablated is attributable specifically to the removal of their baleful influence on local
tissues.