Oxidative Stress in Cardiac Remodeling Post-Ischemia/Reperfusion: Friend or Foe?

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Oxidative Stress in Heart Diseases

Abstract

Acute coronary artery disease remains the leading cause of death in the USA and most westernized cultures. Notwithstanding the promising pharmacological and interventional advances in the treatment of ischemic heart and vascular diseases in the last three decades, the World Health Organization (WHO) estimates that 17.7 million people die yearly from cardiovascular diseases (CVD), representing 31% of all deaths worldwide. More than 75% of CVD deaths, among which 80% are due to heart attacks and strokes, occur in low-income and middle-income countries. Reperfusion following myocardial infarction (MI) is a gold standard intervention that is proven to be highly effective in preventing heart failure development and death. However, reactive oxygen species (ROS) mediated myocardial injury following reperfusion has gained immense attention given its adverse prognostic value. This chapter discusses the mechanisms behind reperfusion induced cardiac injury while focusing on myocardial ROS types, sources and adverse effect. It also highlights the successful mito-targeted antioxidant therapy and touches base on the paradoxal cardioprotective effects of ROS, all within the context of myocardial ischemia/reperfusion (I/R).

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Abbreviations

WHO:

World Health Organization

CVD:

Cardiovascular disease

Ca2+ :

Calcium

ROS:

Reactive Oxygen Species

I/R:

Ischemia Reperfusion

I/RI:

Ischemia-Reperfusion Injury

MI:

Myocardial Infarction

CHD:

Coronary Heart Disease

PCI:

Percutaneous Coronary Intervention

CABG:

Coronary Artery Bypass Grafting

ATP:

Adenosine triphosphate

Na+ :

Sodium

mPTP:

Mitochondrial Permeability Transition Pore

H+ :

Hydrogen ion

NCX:

Na+/Ca2+-exchanger

PKC-δ:

Protein Kinase C delta

PKC-ɛ:

Protein Kinase C epsilon

PARP:

poly (ADP-ribose) polymerase

O2 :

Superoxide anion

XO:

Xanthine oxidase

NADPH:

Nicotinamide Adenine Dinucleotide Phosphate

NOS:

Oxidase Synthase

MPO:

Myeloperoxidase

nNOS:

neuronal NOS

eNOS:

endothelial NOS

iNOS:

inducible NOS

NO:

Nitric Oxide

ONOO :

peroxynitrite

BH4:

tetrahydrobiopterin

H2O2 :

hydrogen peroxide

ETC:

Electron Transport Chain

XDH:

Xanthine dehydrogenase

IL-1:

Interleukine 1

IL-6:

Interleukine 6

TNF-α:

Tumor Necrosis Factor alpha

PMNs:

Polymorphonuclear Lukocytes

HIF-1α:

Hypoxia-inducible factor 1-alpha

MIM:

Mitochondrial Inner Membrane

MnSOD:

Manganese Superoxide Dismutase

H2O2 :

Hydrogen peroxide

MAPKs:

Mitogen-activated Protein Kinases

RAF-MEK:

Rapidly Accelerated Fibrosarcoma- Mitogen-activated protein kinase kinase pathway

PI3K:

PI-3 kinase

HMGB1:

High-mobility box 1

TLRs:

Toll-Like Receptors

NFκB:

Nuclear factor kappa-light-chain-enhancer of activated B cells

PKA:

Protein Kinase A

Akt/PKB:

Protein kinase B

Bcl-2:

B-cell lymphoma 2

MMPs:

Matrix metalloproteinases

BK:

Big Potassium channels

mitoKATP:

Mitochondrial ATP-sensitive K+ channel

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Abidi, E., Kaplan, A., Booz, G.W., Zouein, F.A. (2019). Oxidative Stress in Cardiac Remodeling Post-Ischemia/Reperfusion: Friend or Foe?. In: Chakraborti, S., Dhalla, N., Ganguly, N., Dikshit, M. (eds) Oxidative Stress in Heart Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-13-8273-4_12

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