Attenuating fibrosis
Fibrosis results in scarring of tissues and organs. This may result in the loss of vital functions, ultimately leading to death. Fibrosis is therefore a serious pathological condition. Unfortunately, there are no effective medicines to treat fibrosis.
The hallmark of fibrosis is the excessive production of collagen by myofibroblasts. These myofibroblasts are mostly derived from fibroblasts that are activated by cytokines such as TGFβ. This process can be mimicked in the laboratory in cell cultures. Although there is a vast amount of knowledge about the activation of fibroblasts into myofibroblasts, hardly anything is known whether myofibroblasts can be reversed into normal fibroblasts. If the latter is indeed possible, treatments may even become available for advanced stages of fibrosis (that is, under conditions where many myofibroblasts are present).
We have tested the ability of two low molecular weight molecules (CAPE and ACHP) and one cytokine (IL1β) to inhibit the formation of myofibroblasts out of fibroblasts, and whether myofibroblasts can be reversed into fibroblasts. The same was done with the mixture of products secreted by fetal stem cells, or secreted by stem cells derived from adult fat tissue. It turned out that most of the mentioned components were able to inhibit the activation of fibroblasts into myofibroblasts, and, surprisingly, often also the reversal of myofibroblasts into fibroblasts. Factors secreted by fetal stem cells have a much higher anti-fibrotic potency than the factors secreted by adult stem cells. More research has to be carried to invest treatment possibilities.