Key result
STAT proteins mediate cardioprotective signaling in ischemia-reperfusion injury as potential therapeutic targets.
Why the study?
Key cellular and molecular signalling pathways determining cardiac myocyte fate after ischaemia-reperfusion and myocardial infarction severity have been recently defined, focusing on the STAT family.
STAT signaling in IR injury is better delineated; leaves open targeted Janus kinase modulation for clinical translation.
During the past six years, great progress has been made in defining the key cellular and molecular signalling pathways that determine the fate of cardiac myocytes after ischaemia-reperfusion (IR) and consequently the severity of myocardial infarction. Among the complex network of kinases and transcription factors that mediate signals during IR is the STAT family of 'signal transducers and activators of transcription'. During IR they are inducibly activated by Janus kinases and have the capability of transcriptionally regulating pro-survival and apoptotic gene expression. In this review we focus on recent progress made in elucidating the regulation and role of the STAT family of proteins during cardioprotective signalling events in myocardial preconditioning and during IR injury in cardiac myocyte cells and the myocardium. Moreover, we also highlight developments in understanding how this signalling pathway might be amenable to therapeutic intervention, permitting cardiac myocyte survival following IR.
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Soond et al. (2006) conducted a review in Ischaemia-reperfusion injury and myocardial infarction. STAT signalling pathway was evaluated. The STAT family of proteins plays a key role in cardioprotective signalling during myocardial preconditioning and ischaemia-reperfusion injury, presenting a potential target for therapeutic intervention.
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