Despite recent advances in antibiotic therapy and supportive critical care, sepsis remains a leading cause of death in intensive care units. Currently, the increased vascular permeability is well-recognized to be responsible for inflammation-/sepsis-triggered organ failure and patient mortality.
There is a positive connection between vascular leakage, cardiac depression, and mortality upon sepsis and other inflammation conditions. However, to date, no specific treatment targeting the vascular leak is yet available. Thus, a deeper understanding of mediators and their associated mechanisms in inflammation-/sepsis-triggered-induced vascular leak is of great importance for the development of future therapeutic strategies.
Dr. Fan and his team found a method of reducing the risk of an inflammation-/sepsis-triggered vascular leak, tissue edema or organ dysfunction in a subject. The compelling data suggest that Lcn10 may involve inflammation-/sepsis-induced cardiovascular leak, evidenced by deficiency of Lcn10 increases, whereas therapeutically administration of recombinant truncated Lcn10 protein, reduces cardiovascular permeability and organ injury.