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Sirt3 Mediates the Cardioprotective Effect of Therapeutic Hypothermia after Cardiac Arrest and Resuscitation by Restoring Autophagic Flux via the PI3K/Akt/mTOR Pathway

SIRT3 PI3K/AKT/mTOR通路 自噬 蛋白激酶B 药理学 体温过低 LY294002型 医学 心肺复苏术 心功能曲线 细胞凋亡 化学 内科学 细胞生物学 生物 麻醉 信号转导 复苏 锡尔图因 心力衰竭 生物化学 乙酰化 基因
作者
Hui Wang,Wenwen Wang,Zhiwei Xue,Huiping Gong
出处
期刊:Shock [Ovid Technologies (Wolters Kluwer)]
卷期号:62 (1): 127-138
标识
DOI:10.1097/shk.0000000000002366
摘要

Background : Postresuscitation cardiac dysfunction is a significant contributor to early death following cardiopulmonary resuscitation (CPR). Therapeutic hypothermia (TH) mitigates myocardial dysfunction due to cardiac arrest (CA); however, the underlying mechanism remains unclear. Sirtuin 3 (Sirt3) was found to affect autophagic activity in recent research, motivating us to investigate its role in the cardioprotective effects of TH in the treatment of CA. Methods : Sprague-Dawley rats were used to establish an in vivo CA/CPR model and treated with a selective Sirt3 inhibitor or vehicle. Survival rate, myocardial function, autophagic flux, and Sirt3 expression and activity were evaluated. H9C2 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro . The cells were transfected with Sirt3-siRNA and treated with the autophagy inhibitor chloroquine or the PI3K inhibitor LY294002, and cell viability and autophagic flux were assessed. Results : Rats exhibited decreased survival and impaired cardiac function after CA/CPR, which were alleviated by TH. Mechanistically, TH restored Sirt3 expression and autophagic flux, which were impaired by CA/CPR. Sirt3 inactivation diminished the capacity of TH to restore autophagic flux and partially abolished the improvements in myocardial function and survival. An in vitro study further showed that TH-induced restoration of disrupted autophagic flux by OGD/R was attenuated by pretreatment with Sirt3-siRNA, and this attenuation was partially rescued by the inhibition of PI3K/Akt/mTOR signaling cascades. Conclusions : Sirt3 mediates the cardioprotective effect of TH by restoring autophagic flux via the PI3K/Akt/mTOR pathway. These findings suggest the potential of Sirt3 as a therapeutic target for CA.
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