2012
DOI: 10.1111/j.1478-3231.2012.02775.x
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Oxidative stress rather than triglyceride accumulation is a determinant of mitochondrial dysfunction in in vitro models of hepatic cellular steatosis

Abstract: Our data indicate that ROS formation, rather than cellular steatosis per se, impairs mitochondrial function. Thus, reduction in cellular steatosis may not always be the desired outcome without concomitant improvement in mitochondrial function and/or reducing of ROS formation.

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Cited by 36 publications
(42 citation statements)
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“…Excessive energy substrates available to the hepatocytes can potentially cause cellular steatosis with the increasing generation of free fatty acids (FFA) and ROS, which, in turn, will lead to mitochondrial dysfunction inextricably linked with oxidative stress [19,20]. This is central to the development of dietary-induced NAFLD or TPN-associated liver disease under unbalanced nutrients perturbation and can potentially progress to steatohepatitis, fibrosis and cirrhosis in liver [20,21].…”
Section: Introductionmentioning
confidence: 99%
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“…Excessive energy substrates available to the hepatocytes can potentially cause cellular steatosis with the increasing generation of free fatty acids (FFA) and ROS, which, in turn, will lead to mitochondrial dysfunction inextricably linked with oxidative stress [19,20]. This is central to the development of dietary-induced NAFLD or TPN-associated liver disease under unbalanced nutrients perturbation and can potentially progress to steatohepatitis, fibrosis and cirrhosis in liver [20,21].…”
Section: Introductionmentioning
confidence: 99%
“…This is central to the development of dietary-induced NAFLD or TPN-associated liver disease under unbalanced nutrients perturbation and can potentially progress to steatohepatitis, fibrosis and cirrhosis in liver [20,21]. …”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…In an in vitro study, energy-substrate treatment preserves mitochondrial function unaltered despite higher intracellular triglyceride accumulation. However, mitochondrial function impairment was apparent after 72 h due to ROS formation (Lockman et al, 2012). Therefore, the assessment of changes during short time intervals could be limiting, and prolonged culture times will be necessary to establish a mechanism of NASH development.…”
Section: Discussionmentioning
confidence: 96%
“…The mechanism in HCV infection includes increased lipogenesis, decreased degradation and impaired lipoprotein secretion [30]. Mitochondrial damage by iron-mediated ROS production may affect the lipid metabolism [31].…”
Section: Discussionmentioning
confidence: 99%