Cell membrane repair as a mechanism for ischemic preconditioning?
نویسندگان
چکیده
Since its original description nearly 25 years ago, the phenomenon of ischemic preconditioning (IPC) continues to captivate a great amount of research interest. The ability to render the myocardium resistant to lethal ischemia/reperfusion injury by preconditioning it with a brief episode of ischemia and reperfusion1 has remained largely a laboratory phenomenon, with only a handful of proof-ofconcept clinical studies realizing its true potential.2–4 Of course, the need to apply the IPC protocol before the index myocardial ischemic event has restricted its clinical application to planned cardiac surgery3 or percutaneous coronary intervention,4 settings in which the index myocardial ischemic event can be reliably predicted. The ability to noninvasively reproduce IPC cardioprotection by applying the IPC stimulus to the upper arm or leg with a blood pressure cuff to induce ischemia and reperfusion has also facilitated its clinical translation.3,4 In contrast, interrupting myocardial reperfusion with short-lived episodes of myocardial ischemia, as in ischemic postconditioning,5 an intervention that can be applied at the time of myocardial reperfusion, has been rapidly translated into the clinical setting.6
منابع مشابه
Myocardial remote ischemic preconditioning: from pathophysiology to clinical application.
Short periods of myocardial ischemia followed by reperfusion induce a cardioprotective mechanism when the myocardium is subsequently subjected to a prolonged period of ischemia, a phenomenon known as ischemic preconditioning. As well as its application in the myocardium, ischemic preconditioning can also be induced by brief interruptions of blood flow to other organs, particularly skeletal musc...
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A transient, sublethal ischemic interval confers resistance to a subsequent, otherwise lethal ischemic insult, in a process termed ischemic preconditioning. Poly(ADP-ribose) polymerase-1 (PARP-1) normally functions in DNA repair, but extensive PARP-1 activation is a major cause of ischemic cell death. Because PARP-1 can be cleaved and inactivated by caspases, we investigated the possibility tha...
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ورودعنوان ژورنال:
- Circulation
دوره 121 23 شماره
صفحات -
تاریخ انتشار 2010