Mitochondrial Ca2+ as a key regulator of cell life and death

被引:205
作者
Giacomello, M.
Drago, I.
Pizzo, P.
Pozzan, T.
机构
[1] Univ Padua, Dept Biomed Sci, I-35121 Padua, Italy
[2] Univ Padua, CNR, Inst Neurosci, I-35121 Padua, Italy
[3] Venetian Inst Mol Med, Padua, Italy
关键词
mitochondria; calcium; apoptosis;
D O I
10.1038/sj.cdd.4402147
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Mitochondrial Ca2+ homeostasis is today at the center of wide interest in the scientific community because of its role both in the modulation of numerous physiological responses and because of its involvement in cell death. In this review, we briefly summarize a few basic features of mitochondrial Ca2+ handling in vitro and within living cells, and its involvement in the modulation of Ca2+-dependent signaling. We then discuss the role of mitochondrial Ca2+ in the control of apoptotic death, focusing in particular on the effects of pro- and anti-apoptotic proteins of the Bcl-2 family. Finally, the potential involvement of Ca2+ and mitochondria in the development of two diseases, Ullrich muscular dystrophy and familial Alzheimer's disease, is briefly discussed.
引用
收藏
页码:1267 / 1274
页数:8
相关论文
共 72 条
[1]   Mitochondrial dysfunction in the pathogenesis of Ullrich congenital muscular dystrophy and prospective therapy with cyclosporins [J].
Angelin, Alessia ;
Tiepolo, Tania ;
Sabatelli, Patrizia ;
Grumati, Paolo ;
Bergamin, Natascha ;
Golfieri, Cristina ;
Mattioli, Elisabetta ;
Gualandi, Francesca ;
Ferlini, Alessandra ;
Merlini, Luciano ;
Maraldi, Nadir M. ;
Bonaldo, Paolo ;
Bernardi, Paolo .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (03) :991-996
[2]  
BAFFY G, 1993, J BIOL CHEM, V268, P6511
[3]   Mitochondrial transport of cations: Channels, exchangers, and permeability transition [J].
Bernardi, P .
PHYSIOLOGICAL REVIEWS, 1999, 79 (04) :1127-1155
[4]   ACTIVATION-ENERGIES AND ENTHALPIES DURING CA2+ TRANSPORT IN RAT-LIVER MITOCHONDRIA [J].
BRAGADIN, M ;
POZZAN, T ;
AZZONE, GF .
FEBS LETTERS, 1979, 104 (02) :347-351
[5]   Possible role for mitochondrial calcium in angiotensin II- and potassium-stimulated steroidogenesis in bovine adrenal glomerulosa cells [J].
Brandenburger, Y ;
Kennedy, ED ;
Python, CP ;
Rossier, MF ;
Vallotton, MB ;
Wollheim, CB ;
Capponi, AM .
ENDOCRINOLOGY, 1996, 137 (12) :5544-5551
[6]   A reevaluation of the role of mitochondria in neuronal Ca2+ homeostasis [J].
Budd, SL ;
Nicholls, DG .
JOURNAL OF NEUROCHEMISTRY, 1996, 66 (01) :403-411
[7]  
CARAFOLI E, 1987, ANNU REV BIOCHEM, V56, P395, DOI 10.1146/annurev.biochem.56.1.395
[8]   Bcl-2 and Bax exert opposing effects on Ca2+ signaling, which do not depend on their putative pore-forming region [J].
Chami, M ;
Prandini, A ;
Campanella, M ;
Pinton, P ;
Szabadkai, G ;
Reed, JC ;
Rizzuto, R .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (52) :54581-54589
[9]   Bcl-2 functionally interacts with inositol 1,4,5-trisphosphate receptors to regulate calcium release from the ER in response to inositol 1,4,5-trisphosphate [J].
Chen, R ;
Valencia, I ;
Zhong, F ;
McColl, KS ;
Roderick, HL ;
Bootman, MD ;
Berridge, MJ ;
Conway, SJ ;
Holmes, AB ;
Mignery, GA ;
Velez, P ;
Distelhorst, CW .
JOURNAL OF CELL BIOLOGY, 2004, 166 (02) :193-203
[10]   Quantitative analysis of mitochondrial Ca2+ uptake and release pathways in sympathetic neurons -: Reconstruction of the recovery after depolarization-evoked [Ca2+]i elevations [J].
Colegrove, SL ;
Albrecht, MA ;
Friel, DD .
JOURNAL OF GENERAL PHYSIOLOGY, 2000, 115 (03) :371-388