Sepsis is one of the most common reasons for hospitalisation. This condition is characterised by systemic inflammatory response to infection. International definition of sepsis mainly points out a multi-organ dysfunction caused by a deregulated host response to infection. An uncontrolled inflammatory response, often referred to as “cytokine storm”, leads to an increase in oxidative stress as a result of the inhibition of cellular antioxidant systems. Oxidative stress, as well as pro-inflammatory cytokines, initiate vascular endothelial dysfunction and, in consequence, impair microcirculation. Microcirculation damage leads to adaptive modifications of cell metabolism. Moreover, mitochondrial dysfunction takes place which results in increased apoptosis and impaired autophagy. Non-coding RNA, especially miRNA and lncRNA molecules, may play an important role in the pathomechanism of sepsis. Altered expression of various ncRNAs in sepsis suggest, that these molecules can be used not only as diagnostics and prognostic markers but also as the target points in the pharmacotherapy of sepsis. The understanding of detailed molecular mechanisms leading to organ damage can contribute to the development of specific therapy methods thereby improving the prognosis of patients with sepsis.
Part of the book: Infections and Sepsis Development