Systemic inflammatory response syndrome is triggered by mitochondrial damage

Mitochondria are key organelles of cellular energy metabolism; both mitochondrial function and metabolism determine the physiological function of cells and serve an essential role in immune responses. Key damage-associated molecular patterns (DAMPs), such as mitochondrial DNA and N-formyl peptides, released following severe trauma-induced mitochondrial damage may affect the respiratory chain, enhance oxidative stress and activate systemic inflammatory responses via a variety of inflammation-associated signaling pathways. Severe trauma can lead to sepsis, multiple organ dysfunction syndrome and death. The present review aimed to summarize the pathophysiological mechanisms underlying the effects of human mitochondrial injury-released DAMPs on triggering systemic inflammatory responses and to determine their potential future clinical applications in preventing and treating sepsis.