Role of Mitochondrial Oxidative Stress in Sepsis

IntroductIonDespite the availability of advanced treatments, sepsis is one of the leading causes of death in intensive care units [1,2].Multiple factors contribute to the development of this condition; both extrinsic and intrinsic mechanisms are involved in hemodynamic collapse [3].Extrinsic mechanisms involve endotoxins, viruses, fungi, or other toxins, while intrinsic mechanisms include proinflammatory mediators released by host immune cells.Both of these mechanisms induce a complex cascade of cellular events, resulting in the release of proinflammatory and anti-inflammatory mediators.Sepsis develops after an initial host response to an infection becomes amplified and dysregulated, which leads to circulatory changes and septic shock.The most common consequences are impaired vascular permeability, cardiac malfunction, and mitochondrial dysfunction leading to impaired respiration [4].The pathogenesis of sepsis-induced myocardial injury remains unclear, but the mitochondrial dysfunction of myocardial cells plays a very important role in the pathophysiological mechanism [5]; oxidants and antioxidants also play a key role.Normally, there is a balance between the oxidant and antioxidant systems in the body; oxidative stress occurs when oxidant levels exceed those of antioxidants, which contributes to the septic process and may lead to organ damage.The inflammatory response and persistent oxidative