J Thorac Cardiovasc Surg 2004;128:324-325
© 2004 The American Association for Thoracic Surgery
Reply to the Editor
Gábor Szabó, MD, PhDa,
Csaba Szabó, MD, PhD, DScb
a Department of Cardiac Surgery, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany
b Inotek Pharmaceuticals Corporation, Beverly, MA 01915, USA
| The first 20% of the full text of this article appears below. |
In response to the comments of Bloch and Mehlhorn on the effects of poly–adenosine diphosphate–ribose polymerase (PARP) inhibition after cardioplegic arrest and reperfusion, we agree that the PARP enzyme family has a complex regulatory role under several physiologic and pathologic conditions. After a decade of intensive research, we reported on the role of PARP in general1 and focusing on ischemia-reperfusion injury.2,3 To date, the role of PARP in physiologic DNA repair, apoptosis, and necrosis can be summarized as follows: depending on the severity of DNA damage, genotoxic stimuli can trigger three different pathways. In the case of mild DNA damage, PARP facilitates DNA repair and thus survival. However, the exact physiologic role of PARP still remains to be clarified; many authors have suggested that PARP is an abundant enzyme with limited role under physiologic conditions. More severe DNA damage induces apoptotic cell death, during which caspases, the main executor enzymes of apoptotic process, inactivate PARP, cleaving it into two fragments (p89 and p24) and thus PARP cleavage . . . [Full Text of this Article]
Copyright © 2004 by The American Association for Thoracic Surgery.
