Mobilization of endothelial progenitor cells in sepsis

Sepsis, an intractable clinical syndrome, is often accompanied by severe vascular endothelial injury and barrier dysfunction. Previous evidence has shown that the endogenous repair mechanism of damaged vascular endothelium requires the proliferation of local endothelial cells (ECs), but processes of re-endothelialization and angiogenesis after endothelial injury are also affected by bone marrow-derived endothelial progenitor cells (EPCs). EPC mobilization has been linked to the mechanism of vascular endothelial repair in various chronic diseases. However, the potential value of EPC mobilization in the treatment of sepsis has not been explored.

Literature review was done to summarize the mobilization mechanism of EPC and to describe the cytokines and treatments related to EPC mobilization. Additionally, we summarize what is known about the mechanisms of endothelial damage and repair in sepsis.

During sepsis, many endotoxins and inflammatory factors can damage ECs, resulting in increased vascular permeability and microcirculatory disorders. EPCs can serve as a source of ECs. Increasing evidence suggests that various cytokines and medicines can induce EPC mobilization.

EPC mobilization plays an important role in endothelial repair; this may guide the discovery of novel methods to treat sepsis.