Hypoxia-induced Angiogenesis Rescues Survival from Small for Size Syndrome (SFSS)

After extended hepatectomy, hepatocyte proliferation proceeds sinusoidal endothelial cell (SEC) remodeling causing a transient perturbation of the lobular architecture with proliferating hepatocytes forming avascular, hypoxic, clusters. Hypoxia is, thus, considered at the origin of liver dysfunction in SFSS-hepatectomy. Recently, we showed that activation of hypoxia sensors in an upfront SFSS-hepatectomy surged an early angiogenic switch and preserved the sinusoidal architecture with a favorable impact on survival.