The heart muscle does not regenerate
Scientists went through all the cells in the heart of an adult mouse and found no stem cells among them
Polina Loseva, "The Attic"
One of the recent scandals in the field of regenerative medicine is associated with the name of Harvard biologist Piero Anversa, known as the discoverer of heart stem cells – he was suspected of falsifying data. So there are no stem cells in the heart? A group of Dutch scientists decided to dot all the I's and characterize each cell of the heart separately. They simulated a heart attack and waited for new muscle cells to appear in the damaged area. And they didn't wait.
Stem cells are a group of non–specialized cells in the tissue that are activated only by external stimuli (for example, damage). Multiplying, they renew the tissue or restore it after injuries. However, such cells are not found in all organs: if the liver or blood regenerate well, then everything is very difficult with the nervous tissue, and the retina or pancreas are not subject to restoration at all.
Stem cells could not be detected in the heart for a long time either (although they exist in most other muscles). Until Pietro Anvers appeared, who allegedly discovered the self-renewal of the heart muscle due to stem elements. His discovery inspired great hopes in doctors, and Anvers approved conducting clinical trials using these cells. However, other independent groups failed to reproduce its results, and they demanded the withdrawal of the articles Anvers from scientific journals. Now some of the 31 articles have been withdrawn, and clinical trials have been stopped.
But the question, nevertheless, remained open: are there stem cells in the heart? Dutch scientists have published their answer to this question in the journal PNAS (Kretzschmar et al., Profiling proliferative cells and their progeny in damaged murine hearts). They decided to use the broadest definition of stem cells – as cells that are able to divide and replenish the cellular composition of tissue. And they started searching for these cells in healthy adult mice, in newborn mice and in adult mice who had a heart attack. To make it easier to detect dividing cells, a special line of mice was bred in which the protein Ki-67 – the main marker of dividing cells – was connected to a red fluorescent protein. This made it possible, by disassembling the hearts into individual cells, to isolate only the multiplying cells and study them carefully.
It turned out that there are not many dividing cells in the hearts of mice by themselves. If newborns had slightly less than 10% of all heart cells, then in adults this number barely reached 0.05%.
And even two weeks after a heart attack, when the regeneration processes should be in full force, their number increased only to 0.5%. This fact itself casts doubt on the idea of constant renewal and possible restoration of the heart.
Then the scientists studied the transcriptome (the totality of all the genes working in the cell) of these multiplying cells, each separately. If it was possible to detect dividing muscle cells of the heart in newborns, then in adult mice, even after a heart attack, they could not be found. Instead, fibroblasts (connective tissue cells) and vascular wall cells (endothelium), as well as blood and smooth muscle cells (they are also part of the vessel walls) turned out to be actively dividing fractions. Thus, a close cell-by-cell examination of the heart deprived us of the last hope of finding any stem elements there.
The damaged area of the heart muscle and its enlarged photo. Red is the connective tissue at the site of the injury, green is the intact heart muscle. It can be seen that no new muscle cells are formed at the site of the infarction. © Hubrecht Institute.
But, in order not to leave us without hope at all, the authors of the study point to the important role of the resulting "scar" on the heart. The fibroblasts multiplying in it may not produce muscle cells, but they produce the protein FSTL1, which is found only in the heart of newborn mice. Apparently, it somehow improves the survival of the surrounding heart cells. At least in mice deprived of it, a heart attack is followed by ruptures of the heart muscle. Thus, even if we no longer have to count on a full recovery of the heart muscle, we can at least not prevent its natural overgrowth.
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