Inhibition of the fatty acid oxidation metabolic pathway through inactivation of Cpt1b enhances cardiomyocyte survival and proliferation and allows heart regeneration in adult mice.
During a heart attack, the blood flow that feeds the heart cells is diminished or stopped altogether, killing some of the cells. This is especially problematic since after birth, heart cells pretty much stop multiplying, which makes it difficult for the organism to make new cells to fix the damage.
Not only do the heart cells stop multiplying after birth, they also switch from using sugars to using fat as a source of energy. This switching implies shutting some genes off and turning others on through epigenetic modifications (making some regions of the genome, and thus the genes they harbor, unavailable for the cell).
However, it appears that if you turn off one of the key genes involved in using fat as a source of energy, these heart cells switch back some of the genes involved in cell proliferation on, bringing them back to a more juvenile state where they start multiplying again.
Now, all this is only demonstrated to work in mice so far, but if these results can be replicated in humans, it would open the door to a possible treatment leading to much better outcomes after a heart attack.
Quick summary :
During a heart attack, the blood flow that feeds the heart cells is diminished or stopped altogether, killing some of the cells. This is especially problematic since after birth, heart cells pretty much stop multiplying, which makes it difficult for the organism to make new cells to fix the damage.
Not only do the heart cells stop multiplying after birth, they also switch from using sugars to using fat as a source of energy. This switching implies shutting some genes off and turning others on through epigenetic modifications (making some regions of the genome, and thus the genes they harbor, unavailable for the cell).
However, it appears that if you turn off one of the key genes involved in using fat as a source of energy, these heart cells switch back some of the genes involved in cell proliferation on, bringing them back to a more juvenile state where they start multiplying again.
Now, all this is only demonstrated to work in mice so far, but if these results can be replicated in humans, it would open the door to a possible treatment leading to much better outcomes after a heart attack.
Thank you! Even for someone technical, that needed an ELI5.