Figure 1.

Mitochondrial damage associated molecular patterns (DAMPs). DAMPs derived from mitochondrial components may be released during cellular injury, apoptosis or necrosis. Once these mitochondrial components are released into the extracellular space, they can lead to the activation of innate and adaptive immune cells. The recognition of mitochondrial DAMPs involves toll-like receptors (TLR), formyl peptide receptors (FPR) and purigenic receptors (P2RX7). By binding their cognate ligands or by direct interaction (i.e., reactive oxygen species, ROS), intracellular signaling pathways such as NFkB and the NLRP3 inflammasome become activated resulting in a proinflammatory response. TLR4 = toll-like receptor 4, TLR9 = toll-like receptor 9, P2RX7 = purigenic receptor, FPR1 = formyl peptide receptor 1, NLRP3 = NLR Family Pyrin Domain Containing 3, fMet = N-formylmethionine, mtROS = mitochondrial reactive oxygen species, mtDNA = mitochondrial DNA, Tfam = transcription factor A, mitochondrial, RAGE = receptors for advanced glycation end-products, NFkB = nuclear factor kappa-light-chain-enhancer of activated B cells.