Key result
ACE2 loss in mice exacerbates renal ischemia-reperfusion injury via increased inflammation and oxidative stress.
Why the study?
The role of ACE2 in models of acute kidney injury has not been fully elucidated despite its known beneficial effects in chronic kidney disease.
Does loss of ACE2 exacerbate renal ischemia-reperfusion injury in mice?
Population
Wild-type and ACE2 knock-out mice subjected to renal ischemia-reperfusion injury
Comparison
ACE2 knock-out mice vs wild-type mice
Design
Preclinical experimental study
Follow-up
48 hours after reperfusion
Authors
Loading...
Positions ACE2 as renoprotective in experimental AKI; hypothesis-generating for clinical translation.
Does loss of ACE2 exacerbate renal ischemia-reperfusion injury in mice?
Loss of ACE2 exacerbates inflammation, apoptosis, and oxidative stress in a murine model of acute kidney injury, suggesting a protective role for ACE2.
Fang et al. (2013) studied Acute kidney injury (ischemia-reperfusion injury). Loss of ACE2 (ACE2 knock-out) vs. Wild-type (WT) mice was evaluated on Histologic injury scores, kidney function, inflammatory cell infiltration, cytokine expression, apoptosis, and oxidative stress. Loss of ACE2 in mice exacerbated renal ischemia-reperfusion injury by increasing inflammatory cell infiltration, cytokine expression, apoptosis, and oxidative stress.