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Does Sepsis Cause ‘Double Whammy’ to Endothelial Surface Layer?

June 6, 2017 at 8:51 am

By Paul Schumacker, PhD, editor, American Journal of Respiratory Cell and Molecular Biology

Follow Dr. Schumacker on Twitter @ATSRedEditor

Fibroblast Growth Factor Signaling Mediates Pulmonary Endothelial Gycocalyx Reconstitution

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.”


June Highlights

Perspective: Alveolar Epithelial Cell–Derived Mediators:  Potential Direct Regulators of Large Airway and Vascular Responses

Translational Review: Phosphoinositide 3-Kinase in Asthma:  Novel Roles and Therapeutic Approaches.

Multipotent Myoepithelial Progenitor Cells Are Born Early During Airway Submucosal Gland Development

Genetic Control of Fatty Acid β-Oxidation in Chronic Obstructive Pulmonary Disease

Coupling of Airway Smooth Muscle Bitter Taste Receptors to Intracellular Signaling and Relaxation Is via Gαi1,2,3

Role of Rho-Associated Coiled-Coil Forming Kinase Isoforms in Regulation of Stiffness-Induced Myofibroblast Differentiation in Lung Fibrosis


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