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Metabolic reprogramming and tolerance during sepsis-induced AKI
Hernando Gómez1, John A Kellum1, Claudio Ronco2
1Center for Critical Care Nephrology, Department of Critical Care Medicine, University of Pittsburgh, School of Medicine, Room 604 Scaife Hall, 3550 Terrace Street, Pittsburgh, Pennsylvania 15261, USA.
Nature Reviews. Nephrology
|January 17, 2017
Summary
Host tolerance, the ability to limit inflammation-induced damage, is crucial for fighting infections. Metabolic adaptations are key to immune cell function, influencing outcomes in sepsis-induced acute kidney injury.
Area of Science:
- Immunology
- Metabolic Adaptations
- Sepsis Pathophysiology
Background:
- Host defense involves resistance (limiting pathogen load) and tolerance (limiting tissue damage).
- Metabolic reprogramming is essential for immune cell function during infection.
- Sepsis-induced acute kidney injury (AKI) highlights the critical role of host response.
Purpose of the Study:
- To discuss kidney tolerance mechanisms during sepsis.
- To emphasize the role of metabolic responses in coordinating host defense.
- To propose a novel model for sepsis response and organ protection.
Main Methods:
- Review of current literature on host defense, tolerance, and metabolic adaptations in sepsis-induced AKI.
- Analysis of cellular and organ-level responses to sepsis.
- Conceptual modeling of host-pathogen interactions and metabolic signaling.
Main Results:
- Tolerance is as vital as resistance in determining infection outcomes.
- Metabolic adaptations are central to immune cell function, enabling resistance and tolerance pathways.
- Early metabolic reprogramming in sepsis-induced AKI influences organ dysfunction, fibrosis, and chronic kidney disease development.
Conclusions:
- Metabolic adaptations are critical for coordinating tolerance mechanisms in the kidney during sepsis.
- A novel conceptual model integrating cellular and organic responses to sepsis may guide organ-protective therapies.
- Understanding tolerance and metabolic reprogramming offers new therapeutic targets for sepsis-induced AKI.
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