SR/ER–mitochondrial local communication: Calcium and ROS

Csordás, György; Hajnóczky, György

doi:10.1016/j.bbabio.2009.06.004

Cited by 267 publications

(218 citation statements)

References 197 publications

(229 reference statements)

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“…The FFA present in cells provides a perpetuating and propagating mechanism for oxidative stress via the process of lipid peroxidation and produces large amounts of ROS and free radicals that cause secondary damage to cellular membranes and key organelles, including the ER; additionally, the SERCAs in the membrane of the ER are highly sensitive to ROS (6,52). In our study, we observed distinct alterations in the cytosolic calcium homeostasis after the exposure of the hepatocytes to PA (Fig.…”

Section: Discussionsupporting

confidence: 53%

Enhanced endoplasmic reticulum SERCA activity by overexpression of hepatic stimulator substance gene prevents hepatic cells from ER stress-induced apoptosis

Zhang

Jiang

et al. 2014

American Journal of Physiology-Cell Physiology

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Section: Discussionsupporting

confidence: 53%

Enhanced endoplasmic reticulum SERCA activity by overexpression of hepatic stimulator substance gene prevents hepatic cells from ER stress-induced apoptosis

Zhang

Jiang

et al. 2014

American Journal of Physiology-Cell Physiology

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“…In immune cells such as neutrophils and macrophages, NOX2 (also called gp91phox) is used as a «superoxide gun» to kill pathogens during phagocytosis [30]. In addition to the phagocyte NOX2, six non-phagocytic NOXs have been identified: NOX1, NOX3, NOX4, NOX5, DUOX1 and DUOX2 [31].…”

Section: Source Of Rons In Skeletal Musclementioning

confidence: 99%

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Pierre

Appriou

Gratas-Delamarche

et al. 2016

Free Radical Biology and Medicine

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In the literature, the terms physical inactivity and immobilization are largely used as synonyms. The present review emphasizes the need to establish a clear distinction between these two situations. Physical inactivity is a behavior characterized by a lack of physical activity, whereas immobilization is a deprivation of movement for medical purpose. In agreement with these definitions, appropriate models exist to study either physical inactivity or immobilization, leading thereby to distinct conclusions. In this review, we examine the involvement of oxidative stress in skeletal muscle insulin resistance and atrophy induced by, respectively, physical inactivity and immobilization. A large body of evidence demonstrates that immobilization-induced atrophy depends on the chronic overproduction of reactive oxygen and nitrogen species (RONS). On the other hand, the involvement of RONS in physical inactivity-induced insulin resistance has not been investigated. This observation outlines the need to elucidate the mechanism by which physical inactivity promotes insulin resistance.

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“…Intracellular calcium also activates mitochondrial ATP synthase in rat heart (Das and Harris 1990;Territo et al 2000). Though increased calcium in mitochondria in the presence of excessive iron cannot be explained, ROS may cause calcium change (Csordás and Hajnó czky 2009). A notable consequence of calcium is increased activation of enzymes in the TCA cycle producing NAD(P)H (Hansford and Zorov 1998).…”

Section: Discussionmentioning

confidence: 99%

Temporal changes in mitochondrial activities of rat heart after a single injection of iron, including increased complex II activity

Kim

Song

2010

Animal Cells and Systems

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Male rats were given a single injection of iron, and temporal changes in iron content and iron-induced effects were examined in heart cellular fractions. Over a period of 72 h, the contents of total and labile iron, reactive oxygen species, and NO in tissue homogenate, nuclear debris, and postmitochondrial fractions were mostly constant, but in mitochondria they continuously increased. An abrupt decrease in membrane potential and NAD(P)H at 12 h was also found in mitochondria. The respiratory control ratio was reduced slowly with a slight recovery at 72 h, suggesting uncoupling by iron. While the ATP content of tissue homogenate decreased steadily until 72 h, it showed a prominent increase in mitochondria at 12 h. Total iron and calcium concentration also progressively increased in mitochondria over 72 h. Enzyme activity of the oxidative phosphorylation system was significantly altered by iron injection: activities of complexes I, III, and IV were reduced considerably, but complex II activity and the ATPase activity of complex V were enhanced. A reversal of activity in complexes I and II at 12 h suggested reverse electron transfer due to iron overload. These results support the argument that mitochondrial activities including oxidative phosphorylation are modulated by excessive iron.

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SR/ER–mitochondrial local communication: Calcium and ROS

Cited by 267 publications

References 197 publications

Enhanced endoplasmic reticulum SERCA activity by overexpression of hepatic stimulator substance gene prevents hepatic cells from ER stress-induced apoptosis

Enhanced endoplasmic reticulum SERCA activity by overexpression of hepatic stimulator substance gene prevents hepatic cells from ER stress-induced apoptosis

From physical inactivity to immobilization: Dissecting the role of oxidative stress in skeletal muscle insulin resistance and atrophy

Temporal changes in mitochondrial activities of rat heart after a single injection of iron, including increased complex II activity

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