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Discussion
Acknowledgments
This study was supported by research grants from GX15-070 National Science Council (96-3111-B-075-001-MY3), TVGH (V97B1-006,E1-008,F-001), the VGHUST Joint research Program, and the National Yang-Ming University (Ministry of Education, Aim for the Top University Plan), Taiwan.
Appendix A. Supplementary data
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Keywords
STAT1; STAT3; Apoptosis; Ischemia; Myocardial infarction; Oxidative stress
Introduction
Apoptosis has become increasingly recognized as one mechanism of cell death during ischemia/reperfusion (I/R) injury in cultured cardiac myocytes and in the isolated intact heart [1], [2] and [3]. While research into the underlying molecular mechanisms of I/R remains challenging there is great potential to uncover candidate targets for novel therapeutic intervention through elucidation of the precise signalling cascades that control cell fate following cardiac damage. One of the pathways which is instrumental in determining cell fate following the oxidative stress which occurs during I/R is the JAK-signal transducers and activators of transcription (STAT) factor pathway [4].