Researchers from Israel’s Ben-Gurion University (BGU) in cooperation with the National Institute for Biotechnology of the Negev (NIBN) and the US National Institute of Health (NIH) have made a breakthrough in the fight against lupus – identifying the path used by mitochondrial DNA to exit cells in order to trigger autoimmune diseases and developing a way block that escape route.
Professor Varda Shoshan-Barmatz of the Department of Life Sciences and the founding Director of the NIBN in collaboration with Dr. Jay Chung of the NIH have successfully shown that the mitochondrial protein VDAC1 is "critical" for the release of mitochondrial DNA (mtDNA). mtDNA is linked to the composition of Lupus in patients, in addition, the newly found discovery has shown results in animal model for lupus to successfully relieve symptoms of the disease.
They demonstrated that restricting of VDAC1 with a newly developed molecule resulted in substantial improvement in pathological aspects of the disease.
“When VDAC1 is over-expressed, as found in several diseases, a large pore composed of several VDAC1 units is formed, allowing the release of pro-cell death factors and mtDNA,” BGU explained in a statement.
The new molecule hinders cell death and revitalizes mitochondrial function, helping to combat several diseases, including lupus.
“Our breakthrough is identifying a new pathway for the exit of mitochondrial DNA that we can either trigger under controlled conditions or inhibit using our novel molecule that we specifically developed to prevent the formation of this pathway,” said Shoshan-Barmatz in a statement. “Since the results thus far with lupus have been so promising, we believe that the molecule will be beneficial with regards to other diseases such as Alzheimer’s, Crohn’s and ulcerative colitis - as our preliminary results already support."
