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Updated: Jun 5, 2026
A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
Adenosine generation and signaling during acute kidney injury
Jessica D Bauerle1, Almut Grenz, Jae-Hwan Kim
1Mucosal Inflammation Program, Department of Anesthesiology, University of Colorado Denver, 12700 E 19 Avenue, Mailstop B112, Research Complex 2, Room 7124, Aurora, CO 80045, USA.
Abstract:
Acute kidney injury (AKI) is among the leading causes of morbidity and mortality in hospitalized patients. Particularly in the perioperative period, the most common cause of AKI is renal ischemia. At present, therapeutic modalities to prevent or treat AKI are extremely limited and the search for novel therapeutic interventions for ischemic AKI is an area of intense investigation. Recent studies implicate the endogenous signaling molecule, adenosine, in kidney protection from ischemia. As such, enzymatic production of adenosine from its precursor molecules ATP and AMP, and signaling events through adenosine receptors, play a critical role in attenuating renal inflammation and preserving kidney function during episodes of renal ischemia. Utilizing genetic mouse models with defects in adenosine generation or signaling provide strong evidence for the key role of extracellular adenosine in adapting renal tissues to limited oxygen availability and attenuating hypoxia-driven inflammation of the kidneys. Moreover, experimental therapeutics targeting individual adenosine receptors demonstrate strong prophylactic or therapeutic effects during murine AKI. If these experimental strategies can be translated into a clinical setting, adenosine receptor therapeutics may become an integral part in the prevention or treatment of AKI from renal ischemia.
Insights
Adenosine protects kidneys from ischemia-reperfusion injury by reducing inflammation and preserving function. Targeting adenosine receptors shows promise for preventing and treating acute kidney injury (AKI).
Area of Science:
- Nephrology
- Cardiovascular Research
- Molecular Medicine
Background:
- Acute kidney injury (AKI) is a significant cause of hospital morbidity and mortality.
- Renal ischemia, particularly during the perioperative period, is a primary cause of AKI.
- Current treatments for AKI are limited, necessitating novel therapeutic strategies.
Purpose of the Study:
- To investigate the role of endogenous adenosine in protecting the kidneys against ischemic injury.
- To explore the therapeutic potential of targeting adenosine signaling pathways for AKI treatment.
Main Methods:
- Utilized genetic mouse models with deficiencies in adenosine generation or signaling.
- Examined the effects of extracellular adenosine on renal tissue adaptation to hypoxia.
- Assessed the prophylactic and therapeutic efficacy of experimental adenosine receptor-targeting drugs in murine AKI models.
Main Results:
- Extracellular adenosine plays a critical role in adapting renal tissues to limited oxygen availability.
- Adenosine signaling attenuates hypoxia-driven inflammation in the kidneys.
- Targeting specific adenosine receptors demonstrated significant protective effects in experimental AKI.
Conclusions:
- Adenosine signaling is crucial for kidney protection during renal ischemia.
- Adenosine receptor-targeted therapeutics hold potential for preventing and treating ischemic AKI.
- Translating these findings to clinical practice could offer new therapeutic options for AKI patients.
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