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PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis
Pleckstrin homology‐like domain family A, member 3 (PHLDA3) has a particularly critical role in regulating cell survival under stress conditions. However, whether PHLDA3 plays a role in myocardial ischemia/reperfusion injury has not been studied. We aimed to assess the possible role of PHLDA3 in myocardial ischemia/reperfusion (I/R) injury. PHLDA3 expression was increased in myocardial tissue from rats with myocardial I/R injury and rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury. PHLDA3 knockdown protected against myocardial I/R injury in vivo and H/R injury in vitro. Inhibition of PHLDA3 increased the activation of nuclear factor erythroid‐derived 2‐related factor 2 (Nrf2) associated with regulation of the Akt/glycogen synthase kinase‐3β (GSK‐3β) axis. Repression of Nrf2 reversed PHLDA3‐inhibition‐mediated cardioprotective effects. Taken together, our work demonstrates that PHLDA3 inhibition exerts a protective role in myocardial I/R injury via regulation of the Akt/GSK‐3β/Nrf2 axis. We suggest PHLDA3 as an attractive target for developing treatments against myocardial I/R injury.
PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis
Pleckstrin homology‐like domain family A, member 3 (PHLDA3) has a particularly critical role in regulating cell survival under stress conditions. However, whether PHLDA3 plays a role in myocardial ischemia/reperfusion injury has not been studied. We aimed to assess the possible role of PHLDA3 in myocardial ischemia/reperfusion (I/R) injury. PHLDA3 expression was increased in myocardial tissue from rats with myocardial I/R injury and rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury. PHLDA3 knockdown protected against myocardial I/R injury in vivo and H/R injury in vitro. Inhibition of PHLDA3 increased the activation of nuclear factor erythroid‐derived 2‐related factor 2 (Nrf2) associated with regulation of the Akt/glycogen synthase kinase‐3β (GSK‐3β) axis. Repression of Nrf2 reversed PHLDA3‐inhibition‐mediated cardioprotective effects. Taken together, our work demonstrates that PHLDA3 inhibition exerts a protective role in myocardial I/R injury via regulation of the Akt/GSK‐3β/Nrf2 axis. We suggest PHLDA3 as an attractive target for developing treatments against myocardial I/R injury.
PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis
Meng, Xiaoxue (author) / Zhang, Lu (author) / Han, Bing (author) / Zhang, Zheng (author)
Environmental Toxicology ; 36 ; 2266-2277
2021-11-01
12 pages
Article (Journal)
Electronic Resource
English
Britanin Ameliorates Cerebral Ischemia–Reperfusion Injury by Inducing the Nrf2 Protective Pathway
British Library Online Contents | 2017