Project: STOP SEPSIS
2021-01-01 – 2027-12-31
- Abstract
With 30 million cases, 8 million deaths (3 million children) yearly, sepsis (strongly underfunded) is a huge medical problem. We suggest the innovative principle that sepsis is a failing starvation response which is based on failing key molecules (identified by us) in the liver. The mechanism of their failure, the consequences and therapeutics following form the basis of this project.
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- Journal Article
- open access
Comparative Analysis of Hepatic Gene Expression Profiles in Murine and Porcine Sepsis Models
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- Journal Article
- open access
Sepsis-induced changes in pyruvate metabolism: insights and potential therapeutic approaches
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- Journal Article
- A1
- open access
A critical role for HNF4α in polymicrobial sepsis-associated metabolic reprogramming and death
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- Journal Article
- A1
- open access
Identification and characterization of multiple Paneth cell types in the mouse small intestine
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Paneth cell TNF signaling induces gut bacterial translocation and sepsis
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- Journal Article
- A1
- open access
Crosstalk interactions between transcription factors ERRα and PPARα assist PPARα-mediated gene expression
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- Journal Article
- A1
- open access
The impact of hepatocyte-specific deletion of hypoxia-inducible factors on the development of polymicrobial sepsis with focus on GR and PPARα function
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- Journal Article
- A1
- open access
Mousepost 2.0, a major expansion of the resource
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- Journal Article
- A1
- open access
Hepatic peroxisome proliferator-activated receptor alpha dysfunction in porcine septic shock
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- Journal Article
- A1
- open access
Sepsis : a failing starvation response