Apoptosis in myocardial ischaemia and infarction

Abstract

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.

Figure 1

Overview of the signal transduction pathways related to ischaemia/reperfusion induced apoptosis in cardiomyocytes. In this figure, inducing or activating effects are depicted by an arrow and inhibitory effects are depicted by a blocked line. Akt, protein kinase B; ERK, extracellular signal related kinase; JAK, Janus kinase; JNK, Jun N-terminal kinase; MAPK, mitogen activated protein kinase; NFκB, nuclear factor κB; PI3 kinase, phosphatidylinositol 3`-kinase; ROS, reactive oxygen species; SAPK, stress activated protein kinase; STAT, signal transducer and activator of transcription; TNF, tumour necrosis factor.