The conflicting role of Rac1 in inflammation

Abstract

Inflammatory response is responsible for many pathological events and diseases, characterized by overexpression of pro-inflammatory cytokines. Rac1, a molecule mediating many intracellular signaling pathways, has a tight relationship with inflammation. Over the past decade, many researchers have demonstrated that Rac1 plays a critical role in the initiation and progression of inflammation and sepsis including the cytoskeletal rearrangement, Nox activation and ROS production, activation of NF-κB and release of pro-inflammatory cytokines, phagocytosis, and efferocytosis. In addition, Rac1 is also involved in other mechanisms of inflammation, like angiogenesis, apoptosis, and the invasiveness of the pathogen. Interestingly, Rac1 plays both positive and negative roles in regulating inflammation. Finally, Rac1 as a potent pharmacological target was reviewed. Some clinical and experimental studies showed that inhibition of Rac1 had a protective effect on inflammatory diseases. In summary, all data suggest that Rac1 is a crucial factor in different kinds and stages of inflammatory responses.