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      Redox signaling in cardiac myocytes

      , , , , *
      Free Radical Biology & Medicine
      Elsevier Science
      AIF, apoptosis-inducing factor, ARC, apoptosis repressor with caspase recruitment domain, CamKII, calmodulin kinase II, CTGF, connective tissue growth factor, EB, embryoid body, ECC, excitation–contraction coupling, ER, endoplasmic reticulum, ES, embryonic stem, ETC, electron transport chain, G6PDH, glucose-6-phosphate dehydrogenase, GPCR, G-protein-coupled receptor, HDAC, histone deacetylase, Hif, hypoxia-inducible factor, MAO-A, monoamine oxidase-A, MI, myocardial infarction, MMP, matrix metalloproteinase, MPTP, mitochondrial permeability transition pore, mtDNA, mitochondrial DNA, NCX, Na/Ca exchanger, NOS, nitric oxide synthase, PHD, prolyl hydroxylase dioxygenase, PKA, protein kinase A, PKC, protein kinase C, PKG, protein kinase G, ROS, reactive oxygen species, RyR, ryanodine receptor, SERCA, sarcoplasmic reticulum calcium ATPase, SR, sarcoplasmic reticulum, Trx1, thioredoxin1, TNFα, tumor necrosis factor-α, VEGF, vascular endothelial growth factor, Cardiac myocyte, Reactive oxygen species, Redox signaling, Hypertrophy, Heart failure, NADPH oxidase, Mitochondria, Free radicals

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          The heart has complex mechanisms that facilitate the maintenance of an oxygen supply–demand balance necessary for its contractile function in response to physiological fluctuations in workload as well as in response to chronic stresses such as hypoxia, ischemia, and overload. Redox-sensitive signaling pathways are centrally involved in many of these homeostatic and stress-response mechanisms. Here, we review the main redox-regulated pathways that are involved in cardiac myocyte excitation–contraction coupling, differentiation, hypertrophy, and stress responses. We discuss specific sources of endogenously generated reactive oxygen species (e.g., mitochondria and NADPH oxidases of the Nox family), the particular pathways and processes that they affect, the role of modulators such as thioredoxin, and the specific molecular mechanisms that are involved—where this knowledge is available. A better understanding of this complex regulatory system may allow the development of more specific therapeutic strategies for heart diseases.

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          An ER-mitochondria tethering complex revealed by a synthetic biology screen.

          Communication between organelles is an important feature of all eukaryotic cells. To uncover components involved in mitochondria/endoplasmic reticulum (ER) junctions, we screened for mutants that could be complemented by a synthetic protein designed to artificially tether the two organelles. We identified the Mmm1/Mdm10/Mdm12/Mdm34 complex as a molecular tether between ER and mitochondria. The tethering complex was composed of proteins resident of both ER and mitochondria. With the use of genome-wide mapping of genetic interactions, we showed that the components of the tethering complex were functionally connected to phospholipid biosynthesis and calcium-signaling genes. In mutant cells, phospholipid biosynthesis was impaired. The tethering complex localized to discrete foci, suggesting that discrete sites of close apposition between ER and mitochondria facilitate interorganelle calcium and phospholipid exchange.
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            Cardiac plasticity.

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              Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase.

              The Sod2 gene for Mn-superoxide dismutase (MnSOD), an intramitochondrial free radical scavenging enzyme that is the first line of defense against superoxide produced as a byproduct of oxidative phosphorylation, was inactivated by homologous recombination. Homozygous mutant mice die within the first 10 days of life with a dilated cardiomyopathy, accumulation of lipid in liver and skeletal muscle, and metabolic acidosis. Cytochemical analysis revealed a severe reduction in succinate dehydrogenase (complex II) and aconitase (a TCA cycle enzyme) activities in the heart and, to a lesser extent, in other organs. These findings indicate that MnSOD is required for normal biological function of tissues by maintaining the integrity of mitochondrial enzymes susceptible to direct inactivation by superoxide.

                Author and article information

                Free Radic Biol Med
                Free Radic. Biol. Med
                Free Radical Biology & Medicine
                Elsevier Science
                01 April 2011
                01 April 2011
                : 50
                : 7
                : 777-793
                Cardiovascular Division, King's College London British Heart Foundation Centre, London SE5 9PJ, UK
                Author notes
                [* ]Corresponding author. Fax: +44 20 7346 4771. ajay.shah@ 123456kcl.ac.uk
                © 2011 Elsevier Inc.

                This document may be redistributed and reused, subject to certain conditions.

                Review Article

                Molecular biology
                pkc, protein kinase c,g6pdh, glucose-6-phosphate dehydrogenase,arc, apoptosis repressor with caspase recruitment domain,aif, apoptosis-inducing factor,pka, protein kinase a,ecc, excitation–contraction coupling,nos, nitric oxide synthase,serca, sarcoplasmic reticulum calcium atpase,hif, hypoxia-inducible factor,mi, myocardial infarction,camkii, calmodulin kinase ii,vegf, vascular endothelial growth factor,pkg, protein kinase g,mmp, matrix metalloproteinase,trx1, thioredoxin1,tnfα, tumor necrosis factor-α,ctgf, connective tissue growth factor,mao-a, monoamine oxidase-a,redox signaling,ryr, ryanodine receptor,reactive oxygen species,sr, sarcoplasmic reticulum,cardiac myocyte,ncx, na/ca exchanger,es, embryonic stem,heart failure,ros, reactive oxygen species,hdac, histone deacetylase,nadph oxidase,phd, prolyl hydroxylase dioxygenase,er, endoplasmic reticulum,mitochondria,hypertrophy,mptp, mitochondrial permeability transition pore,mtdna, mitochondrial dna,eb, embryoid body,free radicals,gpcr, g-protein-coupled receptor,etc, electron transport chain


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