Inhibition of mitochondrial permeability transition pore opening: translation to patients

被引:75
作者
Gomez, Ludovic [1 ]
Li, Bo [1 ]
Mewton, Nathan [2 ]
Sanchez, Ingrid [2 ]
Piot, Christophe [3 ,4 ]
Elbaz, Meier [5 ,6 ]
Ovize, Michel [1 ,2 ]
机构
[1] INSERM, Lab Physiol Lyon Nord, U886, F-69373 Lyon, France
[2] Univ Claude Bernard Lyon 1, Hosp Civils Lyon, Lyon, France
[3] INSERM, U661, Montpellier, France
[4] Univ Montpellier I & II, Hop Arnaud Villeneuve, Montpellier, France
[5] Fac Med Toulouse, INSERM, U858, F-31073 Toulouse, France
[6] Univ Toulouse 3, Hop Rangueil, F-31062 Toulouse, France
关键词
Ischaemia; Reperfusion; Postconditioning; Cyclosporine; ISCHEMIA-REPERFUSION INJURY; ACUTE MYOCARDIAL-INFARCTION; NO-REFLOW PHENOMENON; CORONARY-ARTERY; CYCLOPHILIN-D; POSTISCHEMIC REPERFUSION; IRREVERSIBLE INJURY; TRANSMURAL EXTENT; EARLY MINUTES; CYCLOSPORINE;
D O I
10.1093/cvr/cvp063
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
A large body of experimental evidence indicates that during an acute myocardial infarction (AMI), tissue injury occurring after reperfusion represents a significant amount of the whole, irreversible damage. It is now recognized that mitochondrial permeability transition pore opening plays a crucial role in this specific component of myocardial infarction. Ischaemic postconditioning and cyclosporine A (CsA) have been shown to dramatically reduce infarct size in many animal species. Recent proof-of-concept clinical trials support the idea that lethal myocardial reperfusion injury is also of significant importance in patients with ongoing AMI, and that targeting mitochondrial permeability transition by either percutaneous coronary intervention postconditioning or CsA can reduce infarct size and improve the recovery of contractile function after reperfusion. Large-scale trials are ongoing to address whether these new treatments may improve clinical outcome in reperfused AMI patients.
引用
收藏
页码:226 / 233
页数:8
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