The expanded testimony of connective tissue is a problem in chronic maladies of numerous organs, for example, the lungs, liver, kidneys (kidney fibrosis), gut, and the skin. Up to 40 percent of all deaths in modern countries are brought about by the testimony of connective tissue with ensuing tissue scarring. Despite this, there are as of now not many successful medicines accessible.
FAU scientists have now unscrambled a molecular network that controls these procedures and could in future give another approach to treat organ scarring. The outcomes demonstrate that the protein PU.1 causes obsessive deposition of connective tissue.
In connective tissue diseases, for example, systemic sclerosis alluded to altogether as ‘fibrosis’, excessive initiation of connective tissue cells prompts solidifying of the tissue and scarring inside the influenced organ. On a basic level, these infections can influence any organ system and frequently lead to disturbance of organ function.
Connective tissue cells assume a key job in normal injury healing in healthy people. Notwithstanding, if the actuation of connective tissue cells can’t be turned off, fibrotic illnesses happen, in which a gigantic measure of the matrix is deposited in the tissue, prompting scarring and brokenness of the influenced tissue. As of not long ago, researchers did not completely comprehend why to repair forms breakdown in fibrotic ailments.
Scientists can now potentially decipher a molecular mechanism responsible for the ongoing activation of connective tissue cells. In experimental studies, the researchers targeted the protein PU.1. In normal wound healing, the formation of PU.1 is inhibited by the body so that at the end of the normal healing process the connective tissue cells can return to a resting state.
Dr. Andreas Ramming from the Chair of Internal Medicine III at FAU said, “We were able to show that PU.1 is activated in various connective tissue diseases in the skin, lungs, liver, and kidneys. PU.1 binds to the DNA in the connective tissue cells and reprogrammes them, resulting in a prolonged deposition of tissue components.”
“PU.1 is not the only factor involved in fibrosis, as factors that are involved in the deposition of scar tissue have already been identified in the past. What has been discovered now, however, is that PU.1 plays a central role in a network of factors controlling this process.”
“PU.1 is like the conductor in an orchestra if you take it out, the entire concert collapses. This approach has already been tested using an experimental drug, fuelling the hope that clinical trials on inhibiting PU.1 may soon be able to be launched, aimed at treating fibrosis better.”
The scientists have now published their results in the renowned journal Nature.*