Scarring is an unfortunate fact of mammalian life, both following injury and throughout inner organs in old age, when the processes of regeneration and tissue maintenance run awry. Wound healing, or indeed any form of regeneration, is enormously complex. It is a dance of signals and actions carried out between numerous cell populations: various stem cells and progenitor cells; immune cells; somatic cells. These processes are similar at the high level in different tissues, but the details vary. It is far from completely mapped by the research community, as is true of most of cellular metabolism, particularly when multiple cell types are coordinating with one another.
Today’s research is a good illustration of the complexities of regenerative biochemistry. When focusing down on even one class of cell in one tissue, fibroblasts in the skin, a wide variety of phenotypes and activities is revealed. Some of these apparently similar cells have arrived from far away in the body, and have very different roles from their peers of a similar type. If the mechanisms of scarring can be more carefully mapped in this way, there is perhaps the potential to reduce or prevent scars from forming. That would
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