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Feng Wu, PhD

Academic Title:

Research Associate

Primary Appointment:



800 W Baltimore St Baltimore, MD 21201

Phone (Primary):


Education and Training

University of Western Ontario in Canada, PhD, Phyiology, 2005.


Endothelial barrier dysfunction occurs at every stage of acute lung injury (ALI) in severe sepsis, leading to vascular leakage, edema, and respiratory failure.  Our study for the first time uncovered the existence of NOX2/eNOS uncoupling/Rho signaling pathway, which is involved in the mechanism of endothelial barrier dysfunction. RhoA/ROCK activation causes stress fiber formation and plays a central role in the development of endothelial barrier dysfunction and vascular leakage in ALI. 

Hemorrhagic shock (HS) is the leading cause of the deaths associated with traumatic injuries. One of the primary clinical manifestations of HS is the disruption of the vascular barrier, which leads to microvascular hyperpermeability in vital organs such as the lungs. Clinical studies have shown that early resuscitation with fresh frozen plasma (FFP) is associated with improved outcomes including a survival benefit after trauma/HS.  Dr. Kozar for the first time found that the protective effects of FFP resuscitation after HS on lung vascular barrier function are associated with restoration of syndecan-1 and the glycocalyx.  I am now working in Dr. Kozar lab and studying if fibrinogen, the major component of FFP, engages with syndecan-1 to exert the protective effects.  

Research/Clinical Keywords

Septic shock, hemorrhage shock, acute lung injury, vascular leakage, endothelial barrier dysfunction, stress fibers, antioxidants, syndecan-1, fibrinogen, miR-19b,

Highlighted Publications

Wu F, Peng Z, Park PW, Kozar RA. Loss of syndecan-1 abrogates the pulmonary protective phenotype induced by plasma after hemorrhagic shock. Shock. 2017; 48:340-345.

Wu F, Szczepaniak WS, Shiva S, Liu HB, Wang Y, Wang L, Kelley EE, Chen AF, Gladwin MT, McVerry BJ. Nox2-dependent glutathionylation of endothelial NOS leads to uncoupled superoxide production and endothelial barrier dysfunction in acute lung injury. Am J Physiol Lung Cell Mol Physiol.2014; 307:L987-997.

Wu F, Tyml K, Wilson JX. iNOS expression requires NADPH oxidase-dependent redox signaling in microvascular endothelial cells. J Cell Physiol.  2008; 217: 207-214.

Wu F, Wilson JX, Tyml K. Ascorbate protects against impaired arteriolar constriction in sepsis by inhibiting iNOS expression. Free Radic Biol Med. 2004; 37:1282-1289.