Mitoflammation. Mitochondria are targets of stress by many factors, including aging, pathogens, and the environment (e.g., toxins like MPP⁺ and rotenone). Mitochondrial stress can result in the release of damage-associated molecular patterns (DAMPs; shown to the right of the mitochondrion) that activate innate immune receptors and downstream signaling. Ox-mtDNA: oxidized mtDNA. Other DAMPs include reactive oxygen species, ATP, N-formyl peptides, and TFAM. Chronic activation of these pathways results in inflammation and associated pathology. By removing damaged mitochondria, mitophagy is predicted to help prevent mitoflammation. Sliter et al. (2018) indicate that mitophagy prevents activation of the mtDNA–cGAS–STING pathway.