Ischemia-reperfusion Injury and Oxidative Stress

Hepatic Regeneration Under Warm or Cold Ischemia Conditions: Controversies and New Approaches

“…Nonetheless, a two-third partial hepatectomy alone does not cause death in these models, and the remnant liver has the capacity to regenerate. In contrast, 30 min of liver ischemia just before PH exacerbates the remnant liver function, causing high mortality and negatively affecting liver weight restoration [1,17]. It is also well known that vascular occlusion of the hepatic hilum is often used to avoid hemorrhage in liver resection.…”

“…Any surgical situation involving liver hepatectomy requires subsequent regeneration in order to restore the liver/body ratio. The liver's ability to restore tissue after loss depends on the interaction of numerous cells and a complex network of mediators [1]. In most cases, in clinical practice, liver surgery involves both ischemia-reperfusion (I/R) injury and regeneration [1].…”

“…The liver's ability to restore tissue after loss depends on the interaction of numerous cells and a complex network of mediators [1]. In most cases, in clinical practice, liver surgery involves both ischemia-reperfusion (I/R) injury and regeneration [1]. Liver I/R injury is a pathophysiological event that occurs during surgical interventions such as liver resection or liver transplantation (LT); it controls bleeding during parenchymal dissection and has a significant effect on liver function prognosis [2][3][4][5][6].…”

“…I/R injury is a twostage phenomenon in which cell damage due to hypoxia and the lack of biomechanical stimulus is exacerbated upon the restoration of oxygen delivery and shear stress [7]. However, I/R injury is inevitable in liver surgery and significantly reduces the organ's regeneration after hepatectomy [1]. Mechanisms of liver I/R injury are complex; they include mainly microcirculation failure and the related oxidative stress, a series of cellular and molecular responses, and the interaction between hepatocytes, liver sinusoidal endothelial cells, hepatic stellate cells, Kupffer cells, infiltrating neutrophils, macrophages, and platelets [2,[7][8][9][10][11].…”

“…As is well known, the mechanisms of liver damage differ according to the percentage of the liver mass deprived of blood [14]. Therefore, experimental models that reproduce as closely as possible the clinical conditions in which these strategies are applied are likely to lead to the implementation of strategies in clinical practice in the relatively short term [1].…”