Mitochondria and cardioprotection

Lisa, Fabio Di; Canton, Marcella; Menabò, Roberta; Kaludercic, Nina; Bernardi, Paolo

doi:10.1007/s10741-007-9028-z

Cited by 145 publications

(133 citation statements)

References 156 publications

(128 reference statements)

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“…In fact, to generate a proton gradient across the inner membrane, Ca 2þ uptake occurs in mitochondria that utilize oxygen (38)(39)(40)(41) overload also activates calcium-dependent proteases, which could partially degrade contractile proteins. These effects are the basis of a progressive increase of ventricular diastolic pressure (hypercontracture), myocardial stunning, and contraction band necrosis (100,151,170).…”

Section: Ca 2þ Overloadmentioning

confidence: 99%

“…Besides being the moment of ''no-return'' for cell death in reperfusion, mPTP opening is also involved in heart failure development (17,58,127,196). The oxidative opening of mPTP is central in reperfusion injury (for reviews, see [38][39][40][41]158), and, as said, it causes mitochondrial depolarization, loss of small molecular weight substances from the matrix, and rupture of OMM (6,32,126,196). However, experiments with transgenic mice in each of the putative components of mPTP reached controversial results.…”

Section: Mitochondrial Permeability Transition Pore Openingmentioning

confidence: 99%

“…The infarct size reduction by ischemic PostC depends on duration of the index-ischemia, on the number and duration of the brief re-occlusions, and=or on the presence of comorbidities (81,148,174). Further studies should resolve the difference in efficacy of PostC between experimental models and human subjects with comorbidities and=or aging (40,149,155,190).…”

Section: Preconditioning and Postconditioningmentioning

confidence: 99%

“…Although the sources of ROS and RNS within the cells are many, in cardiomyocytes the main sources are mitochondria (38)(39)(40)(41)142). It has been suggested that for massive ROS release the involvement of mPTP is required.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, a positive feedback loop of ''ROS-induced ROS release'' has been suggested (209,210). These organelles may also produce a large quantity of ROS from monoamine oxidase and p66Shc activity (39)(40)(41). Even NOSs can become ''uncoupled'', resulting in the generation of O 2 À and OH instead of NO under certain conditions such as scarcity or absence of the cofactor, tetrahydrobiopterin, and=or of the substrate, L-arginine, as well as in the presence of oxidation of the Zn 2þ -thiolate center of NOS homodimer.…”

Section: Introductionmentioning

confidence: 99%

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Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Pagliaro

Moro

Tullio

et al. 2011

Antioxidants & Redox Signaling

113

152

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Post-ischemic reperfusion may result in reactive oxygen species (ROS) generation, reduced availability of nitric oxide (NO ), Ca 2+ overload, prolonged opening of mitochondrial permeability transition pore, and other processes contributing to cell death, myocardial infarction, stunning, and arrhythmias. With the discovery of the preconditioning and postconditioning phenomena, reperfusion injury has been appreciated as a reality from which protection is feasible, especially with postconditioning, which is under the control of physicians. Potentially cooperative protective signaling cascades are recruited by both pre-and postconditioning. In these pathways, phosphorylative= dephosphorylative processes are widely represented. However, cardioprotective modalities of signal transduction also include redox signaling by ROS, S-nitrosylation by NO and derivative, S-sulfhydration by hydrogen sulfide, and O-linked glycosylation with beta-N-acetylglucosamine. All these modalities can interact and regulate an entire pathway, thus influencing each other. For instance, enzymes can be phosphorylated and=or nitrosylated in specific and=or different site(s) with consequent increase or decrease of their specific activity. The cardioprotective signaling pathways are thought to converge on mitochondria, and various mitochondrial proteins have been identified as targets of these post-transitional modifications in both pre-and postconditioning. Antioxid. Redox Signal. 14, 833-850.

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Section: Ca 2þ Overloadmentioning

confidence: 99%

Section: Mitochondrial Permeability Transition Pore Openingmentioning

confidence: 99%

Section: Preconditioning and Postconditioningmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Pagliaro

Moro

Tullio

et al. 2011

Antioxidants & Redox Signaling

113

152

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Reactive Oxygen Species in the Induction of Toxicity

Lenaz

Strocchi

2009

General, Applied and Systems Toxicology

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Oxidative stress is among the major causes of toxicity due to interaction of reactive oxygen species (ROS) with cellular macromolecules and structures and interference with signal transduction pathways. ROS originate from exogenous and endogenous sources; among the former are UV and ionizing radiation and xenobiotics, the latter are represented by a number of metabolic reactions. The mitochondrial respiratory chain, specially from Complexes I and III, is considered the main origin of ROS particularly under conditions of high membrane potential, but several other sources may be important for ROS generation, such as mitochondrial p66 Shc , monoamine oxidase, α‐ketoglutarate dehydrogenase and extramitochondrial xanthine oxidase, cytochrome P450, nitric oxide synthase, peroxisomal enzymes, plasma membrane NADPH oxidases, and lipoxygenase, with the participation of redox‐active metal ions. ROS are able to oxidatively modify lipids, proteins, carbohydrates and nucleic acids and to activate/inactivate signalling pathways by oxidative modification of redox‐active factors. Cells are endowed with several defence mechanisms, including repair or removal of damaged molecules, and antioxidant systems, either enzymatic or nonenzymatic. Oxidative stress is at the basis of ageing and many pathological disorders, such as ischaemic diseases, neurodegenerative diseases, diabetes and cancer, although the underlying mechanisms are not always completely understood.

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Ischemia/Reperfusion

Kalogeris

Baines

Krenz

et al. 2016

Comprehensive Physiology

619

565

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Ischemic disorders, such as myocardial infarction, stroke, and peripheral vascular disease, are the most common causes of debilitating disease and death in westernized cultures. The extent of tissue injury relates directly to the extent of blood flow reduction and to the length of the ischemic period, which influence the levels to which cellular ATP and intracellular pH are reduced. By impairing ATPase-dependent ion transport, ischemia causes intracellular and mitochondrial calcium levels to increase (calcium overload). Cell volume regulatory mechanisms are also disrupted by the lack of ATP, which can induce lysis of organelle and plasma membranes. Reperfusion, although required to salvage oxygen-starved tissues, produces paradoxical tissue responses that fuel the production of reactive oxygen species (oxygen paradox), sequestration of proinflammatory immunocytes in ischemic tissues, endoplasmic reticulum stress, and development of postischemic capillary no-reflow, which amplify tissue injury. These pathologic events culminate in opening of mitochondrial permeability transition pores as a common end-effector of ischemia/reperfusion (I/R)-induced cell lysis and death. Emerging concepts include the influence of the intestinal microbiome, fetal programming, epigenetic changes, and microparticles in the pathogenesis of I/R. The overall goal of this review is to describe these and other mechanisms that contribute to I/R injury. Because so many different deleterious events participate in I/R, it is clear that therapeutic approaches will be effective only when multiple pathologic processes are targeted. In addition, the translational significance of I/R research will be enhanced by much wider use of animal models that incorporate the complicating effects of risk factors for cardiovascular disease.

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Mitochondria and cardioprotection

Cited by 145 publications

References 156 publications

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Cardioprotective Pathways During Reperfusion: Focus on Redox Signaling and Other Modalities of Cell Signaling

Reactive Oxygen Species in the Induction of Toxicity

Ischemia/Reperfusion

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