adenosine-kinase and Acute-Kidney-Injury
adenosine-kinase has been researched along with Acute-Kidney-Injury* in 3 studies
Reviews
1 review(s) available for adenosine-kinase and Acute-Kidney-Injury
Article | Year |
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"Adenosine an old player with new possibilities in kidney diseases": Preclinical evidences and clinical perspectives.
Renal injury might originate from multiple factors like ischemia reperfusion (I/R), drug toxicity, cystic fibrosis, radio contrast agent etc. The four adenosine receptor subtypes have been identified and found to show diverse physiological and pathological roles in kidney diseases. The activation of A Topics: Acute Kidney Injury; Adenosine; Adenosine Kinase; Animals; Humans; Kidney Diseases; Receptors, Purinergic P1; Reperfusion Injury | 2021 |
Other Studies
2 other study(ies) available for adenosine-kinase and Acute-Kidney-Injury
Article | Year |
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Adenosine kinase inhibition attenuates ischemia reperfusion-induced acute kidney injury.
Acute kidney injury (AKI) has a high morbidity and mortality, and there is no targeted treatment yet. One of the main causes of AKI is ischemia-reperfusion (IR). Increased release of adenosine under stress and hypoxia exerts anti-inflammatory and antioxidant effects. Adenosine kinase (ADK) is an important enzyme that eliminates adenosine in cells, and can maintain low adenosine concentration in cells. Our previous studies have shown that pretreatment of adenosine kinase inhibitor ABT-702 could markedly attenuate cisplatin-induced nephrotoxicity both in vivo and in vitro. This study is designed to investigate the effect of ADK inhibition on IR-induced AKI. The results showed that ADK expression was positively correlated with the degree of renal tubular injury, which suggested that the degree of ADK inhibition reflected the severity of acute tubular necrosis. In vivo, ADK inhibitor could reduce IR-induced renal injury, which might play a protective role by increasing tissue adenosine level, inhibiting oxidative stress, and reducing cell apoptosis. In HK2 cells, cobaltous dichloride (CoCl Topics: Acute Kidney Injury; Adenosine Kinase; Adult; Animals; Apoptosis; Cell Line; Cobalt; Enzyme Inhibitors; Female; Humans; Inflammation; Inosine; Kidney Tubules; Male; Mice, Inbred C57BL; Morpholines; Necrosis; Oxidative Stress; Pyrimidines; Reperfusion Injury | 2020 |
Adenosine kinase inhibition protects against cisplatin-induced nephrotoxicity.
Numerous studies have demonstrated that several mechanisms, including oxidative stress, DNA damage, and inflammatory responses, are closely linked to cisplatin-induced nephrotoxicity. Adenosine, emerging as a key regulatory molecule, is mostly protective in the pathophysiology of inflammatory diseases. A previous study showed that some of the adenosine receptors led to renal protection against ischemia-reperfusion injury. However, these adenosine receptor agonists lack a useful therapeutic index due to cardiovascular side effects. We hypothesized that inhibition of adenosine kinase (ADK) might exacerbate extracellular adenosine levels to reduce cisplatin-induced renal injury. In the present study, pretreatment with the ADK inhibitor ABT-702 could markedly attenuate cisplatin-induced acute kidney injury, tubular cell apoptosis, oxidative stress, and inflammation in the kidneys. Consistent with in vivo results, inhibition of ADK suppressed cisplatin-induced apoptosis, reactive oxygen species production, and inflammation in HK2 cells. Additionally, the protective effect of ADK inhibition was abolished by A Topics: Acute Kidney Injury; Adenosine; Adenosine Kinase; Animals; Apoptosis; Cell Line; Cisplatin; Disease Models, Animal; Humans; Inflammation Mediators; Kidney; Male; Mice, Inbred C57BL; Morpholines; Oxidative Stress; Protein Kinase Inhibitors; Pyrimidines; Reactive Oxygen Species; Receptors, Purinergic P1; Signal Transduction; Up-Regulation | 2019 |