The role of Ca2+ in muscle cell damage

被引:111
作者
Gissel, Hanne [1 ]
机构
[1] Aarhus Univ, Inst Physiol & Biophys, DK-8000 Aarhus C, Denmark
来源
CELL INJURY: MECHANISMS, RESPONSES, AND REPAIR | 2005年 / 1066卷
关键词
calpain; phospholipase A(2); reactive oxygen species; exercise; Duchenne muscular dystrophy; surfactant; skeletal muscle;
D O I
10.1196/annals.1363.013
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Skeletal muscle is the largest single organ of the body. Skeletal muscle damage may lead to loss of muscle function, and widespread muscle damage may have serious systemic implications due to leakage of intracellular constituents to the circulation. Ca2+ acts as a second messenger in all muscle and may activate a whole range of processes ranging from activation of contraction to degradation of the muscle cell. It is therefore of vital importance for the muscle cell to control [Ca2+] in the cytoplasm ([Ca2+](c)). If the permeability of the sarcolemma for Ca2+ is increased, the muscle cell may suffer Ca2+ overload, defined as an inability to control [Ca2+]c. This could lead to the activation of calpains, resulting in proteolysis of cellular constituents, activation of phospholipase A(2) (PLA(2)), affecting membrane integrity, an increased production of reactive oxygen species (ROS), causing lipid peroxidation, and possibly mitochondrial Ca2+ overload, all of which may further worsen the damage in a selfreinforcing process. An increased influx of Ca2+ leading to Ca2+ overload in muscle may occur in a range of situations such as exercise, mechanical and electrical trauma, prolonged ischemia, Duchenne muscular dystrophy, and cachexia. Counteractions include membrane stabilizing agents, Ca2+ channel blockers, calpain inhibitors, PLA2 inhibitors, and ROS scavengers.
引用
收藏
页码:166 / 180
页数:15
相关论文
共 76 条
  • [51] Influence of carbohydrate ingestion on oxidative stress and plasma antioxidant potential following a 3h run
    McAnulty, SR
    McAnulty, LS
    Nieman, DC
    Morrow, JD
    Utter, AC
    Henson, DA
    Dumke, CL
    Vinci, DM
    [J]. FREE RADICAL RESEARCH, 2003, 37 (08) : 835 - 840
  • [52] Loss, restoration, and maintenance of plasma membrane integrity
    McNeil, PL
    Steinhardt, RA
    [J]. JOURNAL OF CELL BIOLOGY, 1997, 137 (01) : 1 - 4
  • [53] MICHALAK M, 1984, J BIOL CHEM, V259, P5540
  • [54] REGULATION OF SKELETAL-MUSCLE SARCOLEMMAL ATP-DEPENDENT CALCIUM-TRANSPORT BY CALMODULIN AND CAMP-DEPENDENT PROTEIN-KINASE
    MICKELSON, JR
    BEAUDRY, TM
    LOUIS, CF
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1985, 242 (01) : 127 - 136
  • [55] THE PLASMA-MEMBRANE CALCIUM-PUMP - A PHYSIOLOGICAL PERSPECTIVE ON ITS REGULATION
    MONTEITH, GR
    ROUFOGALIS, BD
    [J]. CELL CALCIUM, 1995, 18 (06) : 459 - 470
  • [56] PLA2 dependence of diaphragm mitochondrial formation of reactive oxygen species
    Nethery, D
    Callahan, LA
    Stofan, D
    Mattera, R
    DiMarco, A
    Supinski, G
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 2000, 89 (01) : 72 - 80
  • [57] Effects of running distance and training on Ca2+ content and damage in human muscle
    Overgaard, K
    Fredsted, A
    Hyldal, A
    Ingemann-Hansen, T
    Gissel, H
    Clausen, T
    [J]. MEDICINE AND SCIENCE IN SPORTS AND EXERCISE, 2004, 36 (05) : 821 - 829
  • [58] Membrane leakage and increased content of Na+-K+ pumps and Ca2+ in human muscle after a 100-km run
    Overgaard, K
    Lindstrom, T
    Ingemann-Hansen, T
    Clausen, T
    [J]. JOURNAL OF APPLIED PHYSIOLOGY, 2002, 92 (05) : 1891 - 1898
  • [59] Store-operated calcium channels
    Parekh, AB
    Putney, JW
    [J]. PHYSIOLOGICAL REVIEWS, 2005, 85 (02) : 757 - 810
  • [60] EXERCISE CAUSES OXIDATIVE DAMAGE TO RAT SKELETAL-MUSCLE MICROSOMES WHILE INCREASING CELLULAR SULFHYDRYLS
    RAJGURU, SU
    YEARGANS, GS
    SEIDLER, NW
    [J]. LIFE SCIENCES, 1994, 54 (03) : 149 - 157