Key result
ACE2 activation with diminazene aceturate attenuates hyperoxic lung injury in mice via NF-κB and Nrf2.
Why the study?
The study was conducted to investigate the role of angiotensin-converting enzyme 2 in hyperoxic lung injury.
Does ACE2 activation with diminazene aceturate attenuate hyperoxic lung injury in adult mice?
Population
Adult mice exposed to 95% O2
Comparison
ACE2 agonist DIZE vs ACE2 inhibitor MLN-4760 during hyperoxia exposure
Design
Animal experimental study
Follow-up
72 h
Authors
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ACE2 activation attenuates hyperoxic lung injury in mice; hypothesis-generating for human translation, clinical trials required.
Does ACE2 activation with diminazene aceturate attenuate hyperoxic lung injury in adult mice?
Activation of ACE2 attenuates hyperoxic lung injury in mice by inhibiting the NF-κB pathway and activating the Nrf2 pathway.
Fang et al. (2019) studied Hyperoxic lung injury. ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760 vs. Hyperoxia alone was evaluated on Severity of hyperoxic lung injury, inflammatory response, and oxidative stress. In adult mice, activation of ACE2 with diminazene aceturate attenuated hyperoxia-induced lung injury, inflammatory response, and oxidative stress by regulating NF-κB and Nrf2 pathways.
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