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Updated: Jan 22, 2026

RNA Interference-based Investigation of the Function of Heat Shock Protein 27 during Corneal Epithelial Wound Healing
Published on: September 27, 2016
Systemic release of heat-shock protein 27 and 70 following severe trauma
Thomas Haider1, Elisabeth Simader2,3,4, Olaf Glück3,4
1Department of Orthopedics and Trauma Surgery, Medical University of Vienna, Waehringer Guertel 18-20, 1090, Vienna, Austria. thomas.a.haider@meduniwien.ac.at.
Abstract:
Trauma represents a major cause of morbidity and mortality worldwide. The endogenous inflammatory response to trauma remains not fully elucidated. Pro-inflammation in the early phase is followed by immunosuppression leading to infections, multi-organ failure and mortality. Heat-shock proteins (HSPs) act as intracellular chaperons but exert also extracellular functions. However, their role in acute trauma remains unknown. The aim of this study was to evaluate serum concentrations of HSP 27 and HSP 70 in severely injured patients. We included severely injured patients with an injury severity score of at least 16 and measured serum concentration of both markers at admission and on day two. We found significantly increased serum concentrations of both HSP 27 and HSP 70 in severely injured patients. Concomitant thoracic trauma lead to a further increase of both HSPs. Also, elevated concentrations of HSP 27 and HSP 70 were associated with poor outcome in these patients. Standard laboratory parameters did not correlate with neither HSP 27, nor with HSP 70. Our findings demonstrate involvement of systemic release of HSP 27 and HSP 70 after severe trauma and their potential as biomarker in polytraumatized patients.
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