|1.||Ovize, Michel: 19 articles (12/2015 - 01/2005)|
|2.||Yellon, Derek M: 15 articles (10/2014 - 12/2003)|
|3.||Xia, Qiang: 11 articles (03/2014 - 01/2005)|
|4.||Hausenloy, Derek J: 10 articles (01/2015 - 12/2003)|
|5.||Davidson, Sean M: 10 articles (10/2014 - 03/2006)|
|6.||Gao, Qin: 9 articles (11/2010 - 01/2005)|
|7.||Sahach, V F: 9 articles (01/2008 - 01/2002)|
|8.||Molkentin, Jeffery D: 8 articles (05/2015 - 09/2007)|
|9.||Bernardi, Paolo: 7 articles (07/2015 - 05/2007)|
|10.||Argaud, Laurent: 6 articles (10/2014 - 01/2005)|
05/01/2014 - "Recently, the pathophysiology of lower limb ischemia-reperfusion (IR) has been largely improved, acknowledging a key role for mitochondrial dysfunction mainly characterized by impaired mitochondrial oxidative capacity and premature mitochondrial permeability transition pore opening. "
12/01/2015 - "The mitochondrial permeability transition pore (PTP) has been established as an important mediator of ischemia-reperfusion-induced cell death. "
04/01/2015 - "Ischemia-reperfusion (IR) injury leads to mitochondrial permeability transition pore opening, which contributes to cell death. "
01/01/2015 - "In the last twenty years, numerous reports provided solid evidence on the involvement of the mitochondrial permeability transition pore (PTP) in myocardial injury caused by ischemia and reperfusion. "
07/01/2011 - "One of the major mechanisms of cell death in ischemia-reperfusion is suggested to be the opening of a large conductance pore in the inner mitochondrial membrane, known as the mitochondrial permeability transition pore. "
12/01/2015 - "The aims of this study were to evaluate whether the delayed application of low-pressure reperfusion could reduce lethal reperfusion injury and whether the inhibition of the opening of the mitochondrial permeability transition pore is involved in this protection. "
02/01/2008 - "4. The findings of the present study indicate that HSYA protects the myocardium against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. "
01/01/2015 - "Molecular identity of the mitochondrial permeability transition pore and its role in ischemia-reperfusion injury."
10/01/2014 - "HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore."
04/01/2014 - "This protective effect is dependent on its ability to prevent the opening of the mitochondrial permeability transition pore, a critical determinant of cell death in the setting of acute ischaemia-reperfusion injury. "
|3.||Myocardial Ischemia (Ischemic Heart Diseases)
01/01/2003 - "[Factor released during myocardial ischemia reperfusion may become a marker of opening of the mitochondrial permeability transition pore]."
07/07/2015 - "Mcu(-/-) mice display no overt baseline phenotype and are protected against mCa(2+) overload in an in vivo myocardial ischemia-reperfusion injury model by preventing the activation of the mitochondrial permeability transition pore, decreasing infarct size, and preserving cardiac function. "
01/01/2015 - "The mitochondrial permeability transition pore and its role in myocardial ischemia reperfusion injury."
03/01/2014 - "TFES prevents myocardial ischemia/reperfusion injury, and this cardioprotective effect is probably via inhibiting mitochondrial permeability transition pore opening."
10/15/2014 - "Opening of the mitochondrial permeability transition pore (mPTP) appears to be a pivotal event in myocardial ischemia-reperfusion (I/R) injury. "
07/01/2015 - "Reprint of "The mitochondrial permeability transition pore and its adaptive responses in tumor cells"."
12/01/2014 - "The mitochondrial permeability transition pore and its adaptive responses in tumor cells."
01/01/2014 - "The mitochondrial permeability transition pore and cancer: molecular mechanisms involved in cell death."
01/01/2013 - "Mitochondrial permeability transition pore as a selective target for anti-cancer therapy."
10/01/2012 - "Respiratory complexes are believed to play a role in the function of the mitochondrial permeability transition pore (PTP), whose dysregulation affects the process of cell death and is involved in a variety of diseases, including cancer and degenerative disorders. "
01/01/2016 - "As expected, hypothermia treatment decreased mitochondrial permeability transition pore opening and restored the mitochondrial membrane potential and intracellular adenosine triphosphate content. "
02/01/1998 - "The effect of calcium on hypothermia-facilitated resuscitation of warm ischemic kidney tissue slices: a role for the mitochondrial permeability transition pore?"
09/01/2011 - "However, some adjunctive therapies have shown promise in data subanalyses or subpopulations of clinical trials (adenosine, therapeutic hypothermia, and hyperoxemic reperfusion) or in small clinical trials (atrial natriuretic peptide, ischemic postconditioning, and cyclosporine, the mitochondrial permeability transition pore inhibitor). "
|1.||1- Methyl- 4- phenyl- 1,2,3,6- tetrahydropyridine (MPTP)
|2.||Adenosine Triphosphate (ATP)
|7.||Potassium Channels (Potassium Channel)
|2.||Induced Heart Arrest (Cardioplegia)
|3.||Vagus Nerve Stimulation