Modulation of Acetylation: Creating a Pro-survival and Anti-Inflammatory Phenotype in Lethal Hemorrhagic and Septic Shock

Figure 2

Effect of HDACIs on gut-liver/lymph-lung axis in response to hemorrhagic shock. Hemorrhagic shock causes destruction of the gut barrier due to tight junction protein (e.g., claudin-3) loss. Bacteria, endotoxin, and inflammatory cytokines enter into circulation and lung. In the lung tissue, MAPKs are stimulated and neutrophils infiltrated, resulting in acute lung injury. HDACIs block these processing by inhibition of tight junction protein loss in gut and inactivation of MAPKs in lung.