The role of endogenous reactive oxygen species in cardiac myocyte autophagy

Title:

The role of endogenous reactive oxygen species in cardiac myocyte autophagy

Creator:

Wang, J.-P, Chi, R.-F, Li, B, Qin, F.-Z, Han, X.-B, Deng, Y.-Z, and Liu, J

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:395f54bc-1792-424f-8730-d5050d3c6872
uuid:395f54bc-1792-424f-8730-d5050d3c6872
issn:0862-8408

Subject:

fyziologie člověka, human physiology, Reactive oxygen species, Endogenous, Autophagy, Cardiomyocytes, Rats, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

Autophagy is implicated in the maintenance of cardiac homeostasis. Autophagy is activated in heart failure, in which reactive oxygen species (ROS) are increased. Exogenous ROS have been shown to induce cardiomyocyte autophagy alterations. However, little is known about the influences of physiological levels of endogenous ROS on cardiomyocyte autophagy. In the present study, we tested the hypothesis that endogenous ROS in cardiomyocytes play an important role in inducing autophagy. Cultured H9C2 cardiomyocytes or Sprague-Dawley rats were treated with the antioxidant N-acetyl-cysteine (NAC) or the superoxide dismutase mimic tempol under the basal or nutrient deprivation conditions. The autophagic flux was assessed by the lysosomal inhibitor chloroquine. In H9C2 cardiomyocytes, under a basal condition, NAC or tempol increased the ratio of LC3 II/I proteins and reduced LC3 II autophagic flux. Under nutrient deprivation, NAC increased the LC3 II/I ratio and reduced LC3 II autophagic flux. In vivo studies in rats, NAC treatment increased the LC3 II/I ratio and p-Akt protein expression in myocardium. We concluded that the antioxidants reduced autophagic flux in cardiomyocytes under the basal or nutrient deprivation conditions, suggesting that endogenous ROS promote autophagy flux under physiological conditions, and this effect is mediated, at least in part, through Akt inhibition., J.-P. Wang, R.-F. Chi, J. Liu, Y.-Z. Deng, X.-B. Han, F.-Z. Qin, B. Li., and Seznam literatury

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:1

Harvested from:

CDK

Metadata only:

false