Monday, December 12, 2011

Scar formation tells us how to make new therapies

When something in our body gets damaged, repair mechanisms often resort to creating scar tissue. Sometimes this is visible on the outside, on our skin, but it is also present in our organs. The process of scar formation is basically filling up the holes left behind by damaged tissue, that was cleared away by the immune system. The downside of this, is that scar tissue is not functional. In medicine, we would like to stop scar formation, and let the body repair damaged organs by creating new functional tissue. A recent discovery shows how the body forms scars under the influence of mechanical stress. This is an important process, largely responsible for the production of scar tissue in our body. If we can manipulate it, we could reduce scar formation, and therefore cure diseases characterized by excess scar formation, which are pretty common, and collectively known as fibrosis.

Mechanical force
The researchers at Stanford found an enzyme that is involved with the translation of mechanical stress on cells to inflammation and the formation of fibrous tissue that forms a scar. While this might sound strange for cells, mechanical force is present everywhere. For example, there are molecules that attach cells to each other mechanically. Apparently, a significant amount of mechanical force can result in an inflammatory process with corresponding formation of non-functional fibrous tissue. It is the first time mechanical stress has been clearly implied in scarring.

The enzyme
In their experiment the Stanford scientists looked at mice that lacked a specific enzyme, that is activated by mechanical force. They found a decrease in inflammation and fibrosis, the latter being an excess production of fibrous scarring tissue. To further confirm the role of the enzyme, the scientists gave healthy mice a drug that inhibits it, and got the same result. Previously, the enzyme was found to play a role in helping cells become aware of changes in mechanical force, but the researchers at Stanford have shown that is plays a much more profound role in disease processes.

Inflammation and wound healing
When organs get damaged, or wounded, the immune system becomes activated. Damaged and dead cells need to be cleared from the body, and we have specialized cells to do that. In addition, inflammation starts what we call the process of wound healing. Specialized cells form tissue that replaces the damaged or dead cells. This is needed, because otherwise we'd be left with a hole somewhere in our body after clearing cells. However, the immune system and the corresponding wound healing process can go into overdrive, which results in excess formation of fibrous tissue.

When our body produces too much fibrous tissue, we get what we call fibrosis. Too much fibrous tissue can be damaging in itself, because the produced fibres are not functional, but instead function as filler inside organs. This can happen all over the body, highlighting the importance of controlling this process. The most famous example is perhaps what happens after a heart infarct. Damaged tissue is being cleared from the body, and being replaced by scar tissue. However, this leaves the body with a largely dysfunctional heart, as the fibrous tissue is not contributing to the pump function of the heart. Another example is the deadly disease cystic fibrosis, which is still untreatable, even though promising new therapies are being explored.

With the newly discovered mechanism, in which the aforementioned enzyme seems to play a key role, we can possible prevent damage caused by excess fibrous tissue formation and inflammation. Because fibrosis is fairly widespread in the body, and found in a large number of diseases, this could have a big impact in medicine. Time will tell if we are able to develop functional therapies based on this discovery.

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