Cited by 1,062Cardiac Ischemia and ReperfusionOrgan Transplantation Techniques and OutcomesCell death mechanisms and regulation

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Preconditioning the Myocardium: From Cellular Physiology to Clinical Cardiology

YELLON, DEREK M., DOWNEY, JAMES M.·2003·Physiological Reviews

DOI 10.1152/physrev.00009.2003

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Abstract

Yellon, Derek M., and James M. Downey. Preconditioning the Myocardium: From Cellular Physiology to Clinical Cardiology. Physiol Rev 83: 1113-1151, 2003; 10.1152/physrev.00009.2003.—The phenomenon of ischemic preconditioning, in which a period of sublethal ischemia can profoundly protect the cell from infarction during a subsequent ischemic insult, has been responsible for an enormous amount of research over the last 15 years. Ischemic preconditioning is associated with two forms of protection: a classical form lasting ∼2 h after the preconditioning ischemia followed a day later by a second window of protection lasting ∼3 days. Both types of preconditioning share similarities in that the preconditioning ischemia provokes the release of several autacoids that trigger protection by occupying cell surface receptors. Receptor occupancy activates complex signaling cascades which during the lethal ischemia converge on one or more end-effectors to mediate the protection. The end-effectors so far have eluded identification, although a number have been proposed. A range of different pharmacological agents that activate the signaling cascades at the various levels can mimic ischemic preconditioning leading to the hope that specific therapeutic agents can be designed to exploit the profound protection seen with ischemic preconditioning. This review examines, in detail, the complex mechanisms associated with both forms of preconditioning as well as discusses the possibility to exploit this phenomenon in the clinical setting. As our understanding of the mechanisms associated with preconditioning are unravelled, we believe we can look forward to the development of new therapeutic agents with novel mechanisms of action that can supplement current treatment options for patients threatened with acute myocardial infarction.

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The nitric oxide hypothesis of late preconditioning
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Phosphorylation of Tyrosine 182 of p38 Mitogen-activated Protein Kinase Correlates with the Protection of Preconditioning in the Rabbit Heart
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Evidence for Preconditioning by Isoflurane in Coronary Artery Bypass Graft Surgery
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Protein Kinase C- ξ is Responsible for the Protection of Preconditioning in Rabbit Cardiomyocytes
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Direct Inhibition of Cyclooxygenase-1 and -2 by the Kinase Inhibitors SB 203580 and PD 98059
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Ischaemic preconditioning reduces troponin T release in patients undergoing coronary artery bypass surgery.
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Evidence That Late Preconditioning Against Myocardial Stunning in Conscious Rabbits Is Triggered by the Generation of Nitric Oxide
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Ischemic preconditioning triggers the activation of MAP kinases and MAPKAP kinase 2 in rat hearts
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Preconditioning of Human Myocardium With Adenosine During Coronary Angioplasty
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Late preconditioning against myocardial stunning. An endogenous protective mechanism that confers resistance to postischemic dysfunction 24 h after brief ischemia in conscious pigs.
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The mechanism of the tetrazolium reaction in identifying experimental myocardial infarction
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Nicorandil, a potent cardioprotective agent, acts by opening mitochondrial ATP-dependent potassium channels
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Preinfarction Angina as a Predictor of More Rapid Coronary Thrombolysis in Patients with Acute Myocardial Infarction
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Protection of hearts from reperfusion injury by propofol is associated with inhibition of the mitochondrial permeability transition
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The p38‐MAPK inhibitor, SB203580, inhibits cardiac stress‐activated protein kinases/c‐Jun N‐terminal kinases (SAPKs/JNKs)
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Characterisation of the infarct-limiting effect of delayed preconditioning: timecourse and dose-dependency studies in rabbit myocardium
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PKC-dependent activation of p44/p42 MAPKs during myocardial ischemia-reperfusion in conscious rabbits
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Myocardial protection is lost before contractile function recovers from ischemic preconditioning
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Nitric Oxide Donors Induce Late Preconditioning Against Myocardial Stunning and Infarction in Conscious Rabbits via an Antioxidant-Sensitive Mechanism
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Ischemia-Reperfusion of Rat Myocardium Activates Nuclear Factor-κB and Induces Neutrophil Infiltration Via Lipopolysaccharide-Induced CXC Chemokine
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Prospective Temporal Analysis of the Onset of Preinfarction Angina Versus Outcome
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Kidney ischemic preconditioning
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Acute ischaemic preconditioning protects against skeletal muscle infarction in the pig
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Preconditioning does not attenuate myocardial stunning.
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No ischemic preconditioning in heterozygous connexin43-deficient mice
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Involvement of activation of ATP-dependent potassium channels in ischemic preconditioning in swine
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Angina-Induced Protection Against Myocardial Infarction in Adult and Elderly Patients: A Loss of Preconditioning Mechanism in the Aging Heart?
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Cardioprotection at a Distance: Mesenteric Artery Occlusion Protects the Myocardium via an Opioid Sensitive Mechanism
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Demonstration of an early and a late phase of ischemic preconditioning in mice
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Amphetamines induce apoptosis and regulation of bcl‐x splice variants in neocortical neurons
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PI3 Kinase and not p42/p44 Appears to be Implicated in the Protection Conferred by Ischemic Preconditioning
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Acute ischaemic preconditioning protects against skeletal muscle infarction in the pig
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Ischemic Preconditioning Activates MAPKAPK2 in the Isolated Rabbit Heart
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Preconditioning does not prevent postischemic dysfunction in aging heart
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Demonstration of Selective Protein Kinase C–Dependent Activation of Src and Lck Tyrosine Kinases During Ischemic Preconditioning in Conscious Rabbits
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Exogenous nitric oxide can trigger a preconditioned state through a free radical mechanism, but endogenous nitric oxide is not a trigger of classical ischemic preconditioning
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“Isolated rabbit hearts continued to be protected by ischemic preconditioning in the presence of L-NAME, strongly arguing against such a trigger role (247).”
BackgroundSelf-citation
The role of differential activation of p38‐mitogen‐activated protein kinase in preconditioned ventricular myocytes
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Induction of manganese superoxide dismutase in rat cardiac myocytes increases tolerance to hypoxia 24 hours after preconditioning.
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Selective Activation of A3Adenosine Receptors WithN6-(3-Iodobenzyl)Adenosine-5′-N-Methyluronamide Protects Against Myocardial Stunning and Infarction Without Hemodynamic Changes in Conscious Rabbits
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Stress proteins and myocardial protection
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Implications of Prodromal Angina Pectoris in Anterior Wall Acute Myocardial Infarction: Acute Angiographic Findings and Long-Term Prognosis
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Ischemic preconditioning depends on interaction between mitochondrial KATPchannels and actin cytoskeleton
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Direct evidence that protein kinase C plays an essential role in the development of late preconditioning against myocardial stunning in conscious rabbits and that epsilon is the isoform involved.
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"Normothermic range" temperature affects myocardial infarct size
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Dinitrophenol, cyclosporin A, and trimetazidine modulate preconditioning in the isolated rat heart: support for a mitochondrial role in cardioprotection
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Delayed Preconditioning-Mimetic Action of Nitroglycerin in Patients Undergoing Coronary Angioplasty
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Involvement of protein kinase C in the delayed cytoprotection following sublethal ischaemia in rabbit myocardium
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Reduction by Hyaluronidase of Myocardial Necrosis following Coronary Artery Occlusion
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Conscious rabbits become tolerant to multiple episodes of ischemic preconditioning.
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Inducible Nitric Oxide Synthase Modulates Cyclooxygenase-2 Activity in the Heart of Conscious Rabbits During the Late Phase of Ischemic Preconditioning
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Prevention of Ischemic Preconditioning Only by Combined Inhibition of Protein Kinase C and Protein Tyrosine Kinase in Pigs
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RWJ 67657, a Potent, Orally Active Inhibitor of p38 Mitogen-Activated Protein Kinase
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Loss of Preconditioning by Attenuated Activation of Myocardial ATP-Sensitive Potassium Channels in Elderly Patients Undergoing Coronary Angioplasty
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Cardioprotection by opening of the KATPchannel in unstable angina Is this a clinical manifestation of myocardial preconditioning? Results of a randomized study with nicorandil
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Sublethal ischemia alters myocardial antioxidant activity in canine heart
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Inhibition of protein synthesis does not block myocardial protection afforded by preconditioning
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Opening of mitochondrial KATPchannel induces early and delayed cardioprotective effect: role of nitric oxide
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Preconditioning of isolated rabbit cardiomyocytes: induction by metabolic stress and blockade by the adenosine antagonist SPT and calphostin C, a protein kinase C inhibitor
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Direct Preconditioning of Cardiac Myocytes via Opioid Receptors and KATPChannels
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Cardioprotection provided by adenosine receptor activation is abolished by blockade of the KATP channel
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Delta opioid receptor stimulation mimics ischemic preconditioning in human heart muscle
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Sarcolemmal and Mitochondrial Adenosine Triphosphate– dependent Potassium Channels
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Ischemic preconditioning triggers tyrosine kinase signaling: a potential role for MAPKAP kinase 2
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MECHANISMS OF ISCHEMIC PRECONDITIONING
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Inducible Nitric Oxide Synthase Mediates Delayed Myocardial Protection Induced by Activation of Adenosine A 1 Receptors
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Inhibition of Nitric Oxide Synthesis Reduces Infarct Size by an Adenosine-Dependent Mechanism
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Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71.
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Protein Tyrosine Kinase is Downstream of Protein Kinase C for Ischemic Preconditioning's Anti-infarct Effect in the Rabbit Heart
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Activation of Mitochondrial KATPChannel Elicits Late Preconditioning Against Myocardial Infarction via Protein Kinase C Signaling Pathway
Takashi, E., Wang, Y., & Ashraf, M. (1999) · Circulation Research · doi:10.1161/01.res.85.12.1146 · Cited by 151
Preconditioning decreases Bax expression, PMN accumulation and apoptosis in reperfused rat heart
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10.1161/hc4401.098429 · DOI
10.1172/JCI0214270 · DOI
10.1038/sj.bjp.0703594 · DOI

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Authors: YELLON, D. M., & DOWNEY, J. M.
Affiliations: University College Hospital (GB)
ORCID: YELLON, DEREK M.
DOWNEY, JAMES M.
Venue: Physiological Reviews
Publisher: American Physiological Society
Published: 2003-10
Volume: 83
Issue: 4
Pages: 1113-1151
ISSN: 0031-9333 (ISSN-L)
1522-1210
DOI: 10.1152/physrev.00009.2003
OpenAlex: W2047876380
Cited by: 1,062
References: 423
Citations by year: 2026: 9 · 2025: 12 · 2024: 18 · 2023: 17 · 2022: 19 · 2021: 28 · 2020: 23 · 2019: 25 · 2018: 30 · 2017: 30 · 2016: 51 · 2015: 41 · 2014: 41 · 2013: 64 · 2012: 73
FWCI: 8.24
Type: journal article
Language: en
Open access: closed
Locations: Physiological Reviews (publishedVersion)
PubMed (publishedVersion)
UCL Discovery (University College London) (submittedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords: ischemic preconditioning, myocardial infarction, cardioprotection, autacoids, second window of protection, pharmacological preconditioning
MeSH terms: Animals, Humans, Myocardium, Myocardial Ischemia, Ischemic Preconditioning, Myocardial, Myocytes, Cardiac

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Preconditioning the Myocardium: From Cellular Physiology to Clinical Cardiology

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