Fig. 1.

Pathogen-Associated Molecular Patterns (PAMPs) and Damage-Associated Molecular Patterns (DAMPs) interact with cell surface receptors, including Toll-like receptors (TLRs) and other pattern recognition receptors (PRRs), initiating the cascade of mitochondrial dysfunction and inflammation in sepsis [25,26]. Mitochondria within the cell emit reactive oxygen species (ROS) molecules, symbolizing oxidative stress which in turn triggers the formation of the inflammasome, key components such as NOD-like receptors (NLRs), apoptosis-associated speck-like protein (ASC), and procaspase 1 come together, marking the initiation of the inflammatory response [34,35]. Cytokines, such as IL-1β and IL-18, are secreted from the cell and result in mitochondrial damage [36,37]. Fragments of mitochondrial DNA released from the damaged mitochondria act as DAMPs. A feedback loop is formed perpetuating the cycle of inflammation and cellular response. Further mitochondrial damage results in the upregulation of the glycolytic pathway (Warburg effect) [38,39].