Mitochondria and reperfusion injury -: The role of permeability transition

被引:81
作者
Di Lisa, F
Canton, M
Menabò, R
Dodoni, G
Bernardi, P
机构
[1] Univ Padua, CNR, Ist Neurosci, I-35121 Padua, Italy
[2] Univ Padua, Dipartimento Chim Biol, I-35121 Padua, Italy
[3] Univ Padua, Dipartimento Sci Biomed, I-35121 Padua, Italy
关键词
necrosis; apoptosis; NAD; calcium; ischemia;
D O I
10.1007/s00395-003-0415-x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The viability of the ischemic myocardium is jeopardized by alterations, such as ATP decrease and elevation in intracellular [Ca2+], that are related to derangements in mitochondrial function. Besides these established notions, the elucidation of the apoptotic cascade and the availability of novel methodologies for in situ studies prompted new interest in mitochondria. The characterization of mitochondrial channels provided a contribution that is particularly relevant to cardiovascular research. Here we focus on the role of the permeability transition pore by analyzing the methodological requirements for its characterization, the consequences of its opening and the possible relationships with other mitochondrial functions, especially with the K-ATP channels.
引用
收藏
页码:235 / 241
页数:7
相关论文
共 71 条
[1]   Differential actions of cardioprotective agents on the mitochondrial death pathway [J].
Akao, M ;
O'Rourke, B ;
Kusuoka, H ;
Teshima, Y ;
Jones, SP ;
Marbán, E .
CIRCULATION RESEARCH, 2003, 92 (02) :195-202
[2]  
[Anonymous], 1963, ANAL CHEM, DOI DOI 10.1021/AC60201A035
[3]   Ischemic preconditioning depends on interaction between mitochondrial KATP channels and actin cytoskeleton [J].
Baines, CP ;
Liu, GS ;
Birincioglu, M ;
Critz, SD ;
Cohen, MV ;
Downey, JM .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1999, 276 (04) :H1361-H1368
[4]   Contribution of myocyte apoptosis to myocardial infarction? [J].
Bartling, B ;
Holtz, J ;
Darmer, D .
BASIC RESEARCH IN CARDIOLOGY, 1998, 93 (02) :71-84
[5]   Mitochondrial energy dissipation by fatty acids - Mechanisms and implications for cell death [J].
Bernardi, P ;
Penzo, D ;
Wojtczak, L .
VITAMINS AND HORMONES - ADVANCES IN RESEARCH AND APPLICATIONS, VOL 65, 2002, 65 :97-126
[6]   Mitochondria and cell death - Mechanistic aspects and methodological issues [J].
Bernardi, P ;
Scorrano, L ;
Colonna, R ;
Petronilli, V ;
Di Lisa, F .
EUROPEAN JOURNAL OF BIOCHEMISTRY, 1999, 264 (03) :687-701
[7]   Mitochondrial transport of cations: Channels, exchangers, and permeability transition [J].
Bernardi, P .
PHYSIOLOGICAL REVIEWS, 1999, 79 (04) :1127-1155
[8]   A mitochondrial perspective on cell death [J].
Bernardi, P ;
Petronilli, V ;
Di Lisa, F ;
Forte, M .
TRENDS IN BIOCHEMICAL SCIENCES, 2001, 26 (02) :112-117
[9]   Proton selective substate of the mitochondrial permeability transition pore: Regulation by the redox state of the electron transport chain [J].
Broekemeier, KM ;
Klocek, CK ;
Pfeiffer, DR .
BIOCHEMISTRY, 1998, 37 (38) :13059-13065
[10]   Calpain and mitochondria in ischemia/reperfusion injury [J].
Chen, M ;
Won, DJ ;
Krajewski, S ;
Gottlieb, RA .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (32) :29181-29186