REVIEW

Apoptosis in myocardial ischaemia and infarction

P A J Krijnen¹, R Nijmeijer², C J L M Meijer¹, C A Visser⁴, C E Hack³, H W M Niessen¹

¹ Department of Pathology, VU University Medical Centre, PO Box 7075, 1007MB Amsterdam, The Netherlands
² Department of Cardiology, VU University Medical Centre
³ Department of Clinical Chemistry, VU University Medical Centre
⁴ Department of Cardiology, VU University Medical Centre

Correspondence to:
Dr P A J Krijnen, Department of Pathology, VU University Medical Centre, Room nr. 0E16, De Boelelaan 1117, PO Box 7075, 1007MB Amsterdam, The Netherlands;
paj.krijnen{at}vumc.nl

Recent studies indicate that, in addition to necrosis, apoptosis also plays a role in the process of tissue damage after myocardial infarction, which has pathological and therapeutic implications. This review article will discuss studies in which the role and mechanisms of apoptosis in myocardial infarction were analysed in vivo and in vitro in humans and in animals.

Keywords: apoptosis; myocardial ischaemia; myocardial infarction; review

Abbreviations: Akt, protein kinase B; AMI, acute myocardial infarction; ERK, extracellular signal related kinase; ESCM, embryonic stem cell derived cardiomyocytes; HGF, hepatocyte growth factor; HSP, heat shock protein; ICE, interleukin 1ß converting enzyme; IGF-I, insulin-like growth factor I; JAK, Janus kinase; JNK, Jun N-terminal kinase; MAPK, mitogen activated protein kinase; MEKK1, MAPK kinase kinase; MI, myocardial infarction; NFB, nuclear factor B; NO, nitric oxide; PARP, poly(ADP-ribose) polymerase; PI3 kinase, phosphatidylinositol 3`-kinase; SAPK, stress activated protein kinase; STAT, signal transducer and activator of transcription; TGF-ß1, transforming growth factor ß1; TNF, tumour necrosis factor; TUNEL, terminal deoxynucleotidyl transferase mediated dUTP nick end labelling

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