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Mitochondria and cardioprotection

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Abstract

Major factors linking mitochondrial dysfunction with myocardial injury are analyzed along with protective mechanisms elicited by endogenous processes and pharmacological treatments. In particular, a reduced rate of ATP hydrolysis and a slight increase in ROS formation appear to represent the prevailing components of self-defense mechanisms, especially in the case of ischemic preconditioning. These protective processes are activated by signaling pathways, which converge on mitochondria activating the mitochondrial KATP channels and/or inhibiting the mitochondrial permeability transition pore. These pathways can also be stimulated by pharmacological treatments. Another major goal for cardioprotection is decreasing the burst in mitochondrial ROS formation that characterizes post-ischemic reperfusion. Finally, mitochondrial targets for therapeutic intervention may include the switch of substrate being utilized, because inhibition of fatty acid oxidation is associated with cardioprotective effects.

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Abbreviations

AIF:

Apoptosis inducing factor

BH:

BCL-2 homology

CPT:

Carnitine palmitoyl transferase

CsA:

Cyclosporin A

Cx43:

Connexin 43

CyP:

Cyclophilin

Δp:

Protonmotive force

Δψm :

Mitochondrial membrane potential

ER:

Endoplasmic reticulum

FAO:

Fatty acid oxidation

IMM:

Inner mitochondrial membrane

IMS:

Intermembrane space

IPC:

Ischemic preconditioning

MAO:

Monoamine oxidase

mitoKATP :

Mitochondrial KATP channel

Pi:

Inorganic phosphate

OMM:

Outer mitochondrial membrane

PDH:

Pyruvate dehydrogenase

PTP:

Permeability transition pore

ROS:

Reactive oxygen species

SOD:

Superoxide dismutase

PLA2 :

Phospholipase A2

TPP:

Triphenylphosphonium

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Acknowledgements

This work was supported by grants from CNR, FIRB, and MIUR.

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Authors and Affiliations

  1. Dipartimento di Chimica Biologica, Università di Padova, Viale G. Colombo 3, Padova, 35121, Italy

    Fabio Di Lisa, Marcella Canton & Nina Kaludercic

  2. Dipartimento di Scienze Biomediche Sperimentali, Università di Padova, Viale G. Colombo 3, Padova, 35121, Italy

    Paolo Bernardi

  3. Istituto di Neuroscienze del CNR, Università di Padova, Viale G. Colombo 3, Padova, 35121, Italy

    Fabio Di Lisa, Roberta Menabò & Paolo Bernardi

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  1. Fabio Di Lisa
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  2. Marcella Canton
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  3. Roberta Menabò
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Correspondence to Fabio Di Lisa.

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Fabio Di Lisa and Paolo Bernardi are recipients of grants from CNR and MIUR.

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Lisa, F.D., Canton, M., Menabò, R. et al. Mitochondria and cardioprotection. Heart Fail Rev 12, 249–260 (2007). https://doi.org/10.1007/s10741-007-9028-z

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