• Source: Scopus
20092020

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Personal profile

Research interests

We are interested in why patients with severe sepsis develop cellular changes that suggest a failure of cellular housekeeping, which might explain why organ failure ensues in these individuals. A major hypothesis of the lab is that autophagy, a catabolic mechanism involving lysosomal degradation becomes reprogrammed during sepsis and contributes to the changes in cellular composition. An unexpected finding is that autophagy is powerfully influenced by circadian rhythms. Our research seeks to understand the connection between circadian disruption during sepsis and the reprogramming of autophagy. We hope this research will lead to better functional recoveries after critical illness. We particularly focus on lung injury using animal models and are in the process of extending our observations to blood samples from critically ill patients.

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