We recently uncovered how mitochondrial stress, in the form of double stranded breaks in the organelles genetic material (mtDNA), triggers systemic innate immunity. This signaling event is engaged after mitochondrial nucleic acids relocates in the cytoplasm through mitochondrial herniation, a particular form of mitochondrial outer membrane permeabilization.
Inflammation and immunity are known to exert both positive and negative effects on the etiology and the evolution of human diseases. For example, neurodegeneration is triggered by uncontrolled inflammatory responses while the therapeutic effects of standard of care cancer treatments are boosted by systemic immune responses.
Our main interests are to understand the molecular details of herniation and explore the effects of mitochondrial driven innate immunity on the severity of human diseases.
