Abstract
Sepsis is a disordered host response to an infection, and one of its hallmarks is organ failure. Mitochondria appear to be a key actor in the chain of events that results in multiple organ failure and potentially death, despite the pathophysiology being complex and little understood. Apart from supplying energy and metabolic intermediates required for immune cell activation and function, mitochondria also impact inflammation and cell death pathways. These two functions of mitochondria influence immunological responses. Crucially, the stability of end organ metabolism and the efficacy of the immune system are both compromised by mitochondrial dysfunction. A hyperinflammatory state and a lack of cellular homeostasis are further consequences of malfunctioning mitochondria, which also contribute to poor clinical outcomes. Hence, strategies to maximize mitochondrial efficiency are necessary since signs of mitochondrial malfunction are evident even in early stages of sepsis. Replacing or repairing damaged mitochondria may therefore aid in the recovery of organ function in sepsis. Toward the conclusion.
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