Stressed mitochondria leak DNA fragments that induce inflammation.
Oxidative stress drives many disease processes. In mitochondria, in particular, it promotes the release of mitochondrial DNA into surrounding cytosol where it can trigger cellular responses involved in autoimmunity.
A critical aspect of mitochondrial DNA release is the formation of pores created by the oligomerization of specific proteins called voltage-dependent anion channels (VDACs), which are found in the outer mitochondrial membrane. A new study in a mouse model of lupus suggests that inhibition of VDAC oligomerization blocks mitochondrial DNA release, preventing subsequent immune responses.
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These findings suggest that inhibition of VDAC oligomerization may be an alternative therapeutic approach for a wide range of diseases likely associated with mitochondrial DNA release, such as lupus and Parkinson’s disease.