Effects of ischemia and reperfusion on pyruvate dehydrogenase activity in isolated rat hearts☆
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Effects of hypoxia-reoxygenation stress on mitochondrial proteome and bioenergetics of the hypoxia-tolerant marine bivalve Crassostrea gigas
2019, Journal of ProteomicsCitation Excerpt :Phosphorylation of E1 subunit of PDH deactivates the enzyme and thus interrupts the pyruvate supply into the TCA cycle [39,90]. Our present study shows that, similar to mammals [39,90–92] and yeast [90,93], PDH phosphorylation plays an important role in mitochondrial responses to H/R stress in the hypoxia-tolerant bivalve C. gigas. This supports the role of PDH phosphorylation as an ancient and highly conserved mechanism of metabolic regulation during oxygen deficiency.
Defective Branched-Chain Amino Acid Catabolism Disrupts Glucose Metabolism and Sensitizes the Heart to Ischemia-Reperfusion Injury
2017, Cell MetabolismCitation Excerpt :It has long been established that PDH activity is a key determinant for myocardial I-R injury (Lewandowski and White, 1995; Stanley et al., 1997). Cardiac I-R insult is associated with decreased PDH activity and increased fatty acid oxidation; both uncouple glycolysis from glucose oxidation (Kobayashi and Neely, 1983; Liu et al., 1996; Vary and Randle, 1985). Manipulation of PDH activity, such as increasing pyruvate supply, reducing PDH phosphorylation by dichloroacetate (DCA), or partial inhibition of fatty acid oxidation, has been shown to improve I-R injury (Chandler et al., 2003; Kobayashi and Neely, 1983; Lewandowski and White, 1995).
Ascorbic acid prolongs the viability and stability of isolated perfused lungs: A mechanistic study using <sup>31</sup>P and hyperpolarized <sup>13</sup>C nuclear magnetic resonance
2015, Free Radical Biology and MedicineCitation Excerpt :When hypoxic cells are reperfused with oxygenated perfusate (or blood), reactive oxygen species (ROS) form and are generally accepted as the major source of the cellular damage and pulmonary edema that characterize IRI [5–8]. Reperfusion of ischemic lung leads to fundamental metabolic alterations, including a decline in oxidative phosphorylation capacity [9, 10] and reduced activity of the electron transport chain (ETC) complexes [9–12]; in cardiac tissue, ischemia–reperfusion has also been shown to decrease activity of the pyruvate dehydrogenase complex (PDHc) [13, 14]. It is not known, however, whether this energy decline is due solely to the reaction of ischemic lung to reperfusion or whether the EVLP process itself contributes to these changes.
The role of Pyruvate Dehydrogenase Complex in cardiovascular diseases
2015, Life SciencesCitation Excerpt :This in turn reduces the rate of pyruvate and glucose oxidation [55]. There are also studies that have pointed out that during the first 10 to 15 min of reperfusion following transient ischemia in the heart, PDH is predominantly in the phosphorylated inactive form [45,47,73]. Despite the disparity in evidence regarding PDH activity, cardiac efficiency and recovery of contractile function in post-ischemic hearts can be improved by pharmacological stimulation of PDH [5,91], or the infusion of pyruvate [17,62,107].
HS-1793, a recently developed resveratrol analogue protects rat heart against hypoxia/reoxygenation injury via attenuating mitochondrial damage
2013, Bioorganic and Medicinal Chemistry Letters
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Supported by NIH grant No. HL-18206.
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Present address: Department of Medicine, Harvard Medical School, 02115, USA.