Researchers have struggled to capture how mitochondrial DNA escapes the mitochondria—the energy powerhouse—in living cells. But now, a study published in the journal Science, provides an understanding of this process and could explain how inflammation occurs in autoimmune diseases.
The mechanism involves the mitochondrial voltage-dependent anion channel (VDAC1) protein that, when several units come together, forms a large pore on the mitochondrial outer membrane. This pore promotes cell death signals and the release of mitochondrial DNA, triggering inflammation as seen in Lupus.
Additionally, researchers developed a molecule to block VDAC pore formation and, in turn, prevent cell death, mitochondrial DNA from exiting the mitochondria, and restore the organelle’s function.
Jay H. Chung, Ph.D., M.D., senior investigator in the Laboratory of Obesity and Aging Research at NHLBI and study author, hopes that blocking this mechanism can be applied to other disease states. “We hope to further study the role of VDAC pore formation not only in classical autoimmune diseases, but in inflammation-associated diseases like atherosclerosis and cardiovascular diseases.”
NHLBI partly funded this study.