{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T22:36:51Z","timestamp":1792708611519,"version":"4.5.0"},"reference-count":221,"publisher":"Oxford University Press (OUP)","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,8,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Ischaemic postconditioning (brief periods of ischaemia alternating with brief periods of reflow applied at the onset of reperfusion following sustained ischaemia) effectively reduces myocardial infarct size in all species tested so far, including humans. Ischaemic postconditioning is a simple and safe manoeuvre, but because reperfusion injury is initiated within minutes of reflow, postconditioning must be applied at the onset of reperfusion. The mechanisms of protection by postconditioning include: formation and release of several autacoids and cytokines; maintained acidosis during early reperfusion; activation of protein kinases; preservation of mitochondrial function, most strikingly the attenuation of opening of the mitochondrial permeability transition pore (MPTP). Exogenous recruitment of some of the identified signalling steps can induce cardioprotection when applied at the time of reperfusion in animal experiments, but more recently cardioprotection was also observed in a proof-of-concept clinical trial. Indeed, studies in patients with an acute myocardial infarction showed a reduction of infarct size and improved left ventricular function when they underwent ischaemic postconditioning or pharmacological inhibition of MPTP opening during interventional reperfusion. Further animal studies and large-scale human studies are needed to determine whether patients with different co-morbidities and co-medications respond equally to protection by postconditioning. Also, our understanding of the underlying mechanisms must be improved to develop new therapeutic strategies to be applied at reperfusion with the ultimate aim of limiting the burden of ischaemic heart disease and potentially providing protection for other organs at risk of reperfusion injury, such as brain and kidney.<\/jats:p>","DOI":"10.1093\/cvr\/cvq129","type":"journal-article","created":{"date-parts":[[2010,5,6]],"date-time":"2010-05-06T21:52:45Z","timestamp":1273182765000},"page":"406-423","source":"Crossref","is-referenced-by-count":461,"title":["Postconditioning and protection from reperfusion injury: where do we stand?Position Paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology"],"prefix":"10.1093","volume":"87","author":[{"given":"Michel","family":"Ovize","sequence":"first","affiliation":[{"name":"1 \u00a0Service d'Explorations Fonctionnelles Cardiovasculaires and Inserm U886, Hospices Civils de Lyon, University of Lyon, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gary F.","family":"Baxter","sequence":"additional","affiliation":[{"name":"Cardiff University 2 \u00a0 Division of Pharmacology, The Welsh School of Pharmacy , , King Edward VII Avenue, Cardiff CF10 3NB ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabio","family":"Di Lisa","sequence":"additional","affiliation":[{"name":"Universit\u00e0 di Padova 3 \u00a0 Dipartimento di Chimica Scienze Biomediche Sperimentali , , Viale G. Colombo 3, Padova 35131 ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P\u00e9ter","family":"Ferdinandy","sequence":"additional","affiliation":[{"name":"University of Szeged 4 \u00a0 Cardiovascular Research Group, Department of Biochemistry , , D\u00f3m t\u00e9r 9, H-6720 Szeged ,","place":["Hungary"]},{"name":"University of Szeged 5 \u00a0 Pharmahungary Group, Department of Biochemistry , , Hajn\u00f3czy utca 6, H-6722 Szeged ,","place":["Hungary"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Garcia-Dorado","sequence":"additional","affiliation":[{"name":"Hospital Universitary Vall d'Hebron 6 \u00a0 , P masculine Vall d'Hebron 119, Barcelona 08035 ,","place":["Spain"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek J.","family":"Hausenloy","sequence":"additional","affiliation":[{"name":"University College London Hospital & Medical School 7 \u00a0 Hatter Cardiovascular Institute, Centre for Cardiology & Research Department of Cardiovascular Medicine , , 67 Chenies Mews, London WC1E 6HX ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerd","family":"Heusch","sequence":"additional","affiliation":[{"name":"University of Essen, Medical School 8 \u00a0 Institute for Pathophysiology , , Hufelandstrasse 55, 45122 Essen ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jakob","family":"Vinten-Johansen","sequence":"additional","affiliation":[{"name":"Carlyle Fraser Heart Center, Emory University Hospital Midtown and Emory University 9 \u00a0 , 550 Peachtree Street NE, Atlanta, GA 30308-2225 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Derek M.","family":"Yellon","sequence":"additional","affiliation":[{"name":"University College London Hospital & Medical School 7 \u00a0 Hatter Cardiovascular Institute, Centre for Cardiology & Research Department of Cardiovascular Medicine , , 67 Chenies Mews, London WC1E 6HX ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rainer","family":"Schulz","sequence":"additional","affiliation":[{"name":"University of Essen, Medical School 8 \u00a0 Institute for Pathophysiology , , Hufelandstrasse 55, 45122 Essen ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,5,6]]},"reference":[{"key":"2026080915142431300_CVQ129C1","doi-asserted-by":"crossref","first-page":"133","DOI":"10.1056\/NEJM197107152850301","article-title":"Myocardial changes associated with cardiogenic shock","volume":"285","author":"Page","year":"1971","journal-title":"N Engl J Med"},{"key":"2026080915142431300_CVQ129C2","doi-asserted-by":"crossref","first-page":"640","DOI":"10.1161\/01.CIR.46.4.640","article-title":"Estimation of infarct size in man and its relation to prognosis","volume":"46","author":"Sobel","year":"1972","journal-title":"Circulation"},{"key":"2026080915142431300_CVQ129C3","doi-asserted-by":"crossref","first-page":"30","DOI":"10.1016\/S0735-1097(01)01711-9","article-title":"The relationships of left ventricular ejection fraction, end-systolic volume index and infarct size to six-month mortality after hospital discharge following myocardial infarction treated by thrombolysis","volume":"39","author":"Burns","year":"2002","journal-title":"J Am Coll Cardiol"},{"key":"2026080915142431300_CVQ129C4","first-page":"186","article-title":"Increase of myocardial salvage and left ventricular function recovery with intracoronary abciximab downstream of the coronary occlusion in patients with acute myocardial infarction treated with primary coronary intervention","volume":"62","author":"Bellandi","year":"2004","journal-title":"Catheter Cardiovasc Interv"},{"issue":"Suppl. 1","key":"2026080915142431300_CVQ129C5","doi-asserted-by":"crossref","first-page":"SI3","DOI":"10.1016\/S0140-6736(98)90012-5","article-title":"Epidemiology of heart failure and ventricular dysfunction","volume":"352","author":"Sharpe","year":"1998","journal-title":"Lancet"},{"key":"2026080915142431300_CVQ129C6","doi-asserted-by":"crossref","first-page":"786","DOI":"10.1161\/01.CIR.56.5.786","article-title":"The wavefront phenomenon of ischemic cell death. 1. 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