[ad_1]
The increased deposition of connective tissue is a problem in chronic diseases of many organs such as the lungs (idiopathic pulmonary fibrosis), liver (cirrhosis), kidney (kidney fibrosis), intestines (graft disease against the lungs). host) and skin (systemic scleroderma). ).
In industrialized countries, nearly 40% of deaths are due to deposition of connective tissue and scarring of tissues. Despite this, there are currently very few effective treatments available.
Scientists from the FAU, Department of Medicine 3 – Rheumatology and Immunology, led by Professor Georg Schett, have now deciphered a molecular network that controls these processes and could in the future be a new way to treat scars of 39; organs. The results show that the PU.1 protein causes a pathological deposition of the connective tissue. Scientists have now published their findings in Nature.
In connective tissue diseases such as systemic scleroderma, collectively referred to as "fibrosis", excessive activation of connective tissue cells leads to hardening of the tissue and scarring of the affected organ. In principle, these diseases can affect any organic system and very often cause a disruption of the functioning of the organ. Connective tissue cells play a key role in the normal healing of wounds in healthy individuals. However, if the activation of connective tissue cells can not be disabled, fibrotic diseases appear in which an enormous amount of matrix is deposited in the tissue, resulting in scarring and dysfunction of the affected tissue. Until now, scientists did not really understand why repair processes worked poorly in fibrotic diseases.
An international team of scientists led by Dr. Andreas Ramming of the FAU Chair of Internal Medicine III has now been able to decipher a molecular mechanism responsible for the ongoing activation of connective tissue cells. In experimental studies, the researchers targeted the PU.1 protein. During normal healing of wounds, the body inhibits the formation of PU.1, so that at the end of the normal healing process, the connective tissue cells can return to the resting state.
"We have been able to show that PU.1 is activated in various connective tissue diseases of the skin, lungs, liver and kidneys. PU.1 binds to the DNA of connective tissue cells and reprograms them, resulting in prolonged deposition of tissue components, "says Dr. Ramming. PU.1 is not the only factor involved in fibrosis because factors involved in the deposition of scar tissue have already been identified in the past. What has been discovered now is that PU.1 plays a central role in a network of factors controlling this process. "PU.1, it's like the orchestra leader," says Ramming, "if you remove it, it's all the concert that's going to collapse." This approach has already been tested with an experimental drug, fueling the hope that clinical trials on the inhibition of PU. 1 could soon be launched to better treat fibrosis.
This article has been republished from documents provided by the University of Erlangen-Nuremberg. Note: Content may have changed for length and content. For more information, please contact the cited source.
Reference:
Wohlfahrt, T., Rauber, S., Uebe, S., Luber, M., Soare, A., Ekici, A.,. . . Ramming, A. (2019). PU.1 controls fibroblast polarization and tissue fibrosis. Nature. doi: 10.1038 / s41586-019-0896-x
[ad_2]
Source link
