The endothelial surface layer (ESL) is critical to vascular function. During sepsis, ESL is degraded, causing septic lung injury.

In their June American Journal of Respiratory Cell and Molecular Biology article, Yimu Yang, MD, PhD, and colleagues report on experiments with human samples and animal models.

The authors found that following non–septic pulmonary ESL degradation, “rapid, homeostatic ESL reconstitution” occurred, “mediated by endothelial induction of fibroblast growth factor receptor 1 (FGFR1) expression.” However, the researchers learned, ESL reconstitution is impaired during sepsis, coincident with loss of EGFR1 expression, suggesting that “sepsis may cause vascular injury not only by triggering ESP degradation but also by impairing ESL reconstitution.”

The article is titled, "Fibroblast Growth Factor Signaling Mediates Pulmonary Endothelial Gycocalyx Reconstitution."