Role of cellular energetics in ischemia-reperfusion and ischemic preconditioning of myocardium

Hassinen, Ilmo E.; Vuorinen, Klaus; Ylitalo, Kari; Ala-Rämi, Antti

doi:10.1007/978-1-4615-5653-4_26

Cited by 10 publications

(14 citation statements)

References 35 publications

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“…Also, under acute cholestasis induced by short-term bile duct ligation in rat, the level of IF1 was found increased at the liver plasma membrane, indicating that the IF1-traffi cking pathway might be regulated by hepatobiliary cholesterol metabolism ( 30 ). Moreover, mobilization of mitochondrial IF1 in cardiomyocytes in response to experimental ischemia has been previously reported ( 31,32 ); hence, serum IF1 concentration might partly refl ect a subtle balance between its utilization and release, depending on the cell energetic status. Finally, environmental factors, which are known to modulate HDL levels, had little or no infl uence on IF1 concentrations, suggesting that individual factors (genetic and metabolic) might control serum IF1 levels.…”

Section: Discussionmentioning

confidence: 73%

Serum IF1 concentration is independently associated to HDL levels and to coronary heart disease: the GENES study

Genoux

Ruidavets

Ferrières

et al. 2013

Journal of Lipid Research

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Section: Discussionmentioning

confidence: 73%

Serum IF1 concentration is independently associated to HDL levels and to coronary heart disease: the GENES study

Genoux

Ruidavets

Ferrières

et al. 2013

Journal of Lipid Research

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“…Traditionally, creatine kinase has been assumed to serve as the sole intracellular energy transport mechanism [4,8,10,42]. Recent studies in muscles with genetically or pharmacologically disrupted creatine kinase indicate, however, that energy transfer does not exclusively rely on this enzyme [43,45,46,47•].…”

Section: High-energy Phosphoryl Transfermentioning

confidence: 99%

Failing energetics in failing hearts

et al. 2000

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The perpetual and vigorous nature of heart muscle work requires efficient myocardial energetics. This depends not only on adequate ATP production, but also on efficient delivery of ATP to muscle ATPases and rapid removal of ADP and other by-products of ATP hydrolysis. Indeed, recent evidence indicates that defects in communication between ATP-producing and ATP-consuming cellular sites are a major factor contributing to energetic deficiency in heart failure. In particular, the failing myocardium is characterized by reduced catalytic activity of creatine kinase, adenylate kinase, carbonic anhydrase, and glycolytic enzymes, which collectively facilitate ATP delivery and promote removal of ADP, Pi, and H+ from cellular ATPases. Although energy transfer through adenylate kinase and glycolytic enzymes has been recognized as an adaptive mechanism supporting compromised muscle energetics, in the failing myocardium the total compensatory potential of these systems is diminished. A gradual accumulation of defects at various steps in myocardial energetic signaling, along with compromised compensatory mechanisms, precipitates failure of the whole cardiac energetic system, ultimately contributing to myocardial dysfunction. These advances in our understanding of the molecular bioenergetics in heart failure provide a new perspective toward improving the energetic balance of the failing myocardium.

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“…3 It is generally established that ischaemic preconditioning can exert beneficial effects also on cardiac energetics, especially during reperfusion. 4,5 Although this manoeuvre preserves the myocardial levels of high energy phosphates, 6 it is not clear whether this is due to the participation of an increased number of viable cells contributing to cardiac energetics, or to an additional intrinsic ability of mitochondria to produce adequate amounts of ATP. For instance, while some findings suggest that oxygen consumption rate 7 and adenyl nucleotide transferase activity 8 are preserved after reperfusion in the preconditioned hearts, other works show that mitochondrial respiration/phosphorylation coupling is unchanged, 9 or even impaired.…”

Section: Introductionmentioning

confidence: 99%

Ischemic preconditioning preserves proton leakage from mitochondrial membranes but not oxidative phosphorylation during heart reperfusion

Muscari

Bonafè

Gamberini

et al. 2005

Cell Biochemistry & Function

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The aim of this study was to evaluate the role of mitochondria in the recovery of cardiac energetics induced by ischaemic preconditioning at reperfusion. Isolated rat hearts were aerobically perfused (control), subjected to global ischaemia and reperfusion (reperfusion), or subjected to 3 brief cycles of ischaemia/reperfusion and then to the protocol of reperfusion (preconditioning). At the end of the perfusion, antimycin A was delivered to the heart for 25 min, to inhibit mitochondrial respiration and stimulate glycolysis. The increased amount of lactate released in the coronary effluent was correlated with the number of viable cells producing this end-product of glycolysis. Preconditioned hearts released 18% more lactate than reperfused hearts (p < 0.05). This result indicates that preconditioning partially preserved cell viability, as was also evidenced by the MTT assay performed on cardiac biopsies. The difference between antimycin A-stimulated and basal lactate concentration, representing the contribution of mitochondria to the overall energetics of cardiac tissue, was also 18% more elevated in the preconditioned hearts than in the reperfused hearts (p < 0.01). The study of the respiratory function of mitochondria isolated at the end of perfusion, showed that preconditioning did not improve the oxygen-dependent production of ATP (state 3 respiration, ADP/O). On the contrary, state 4 respiration, which is related to proton leakage, was 35.0% lower in the preconditioned group than reperfusion group (p < 0.05). Thus, preconditioning ameliorates cardiac energetics by preserving cell death, but without affecting mitochondrial oxidative phosphorylation. Mitochondria can contribute to cell survival by the attenuation of proton leak from inner membrane.

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Role of cellular energetics in ischemia-reperfusion and ischemic preconditioning of myocardium

Cited by 10 publications

References 35 publications

Serum IF1 concentration is independently associated to HDL levels and to coronary heart disease: the GENES study

Serum IF1 concentration is independently associated to HDL levels and to coronary heart disease: the GENES study

Failing energetics in failing hearts

Ischemic preconditioning preserves proton leakage from mitochondrial membranes but not oxidative phosphorylation during heart reperfusion

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