Altered cardiac calcium handling in diabetes

被引：83

作者：

Belke, DD ^{[1
]}

Dillmann, WH ^{[1
]}

机构：

[1] Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA

来源：

CURRENT HYPERTENSION REPORTS | 2004年 / 6卷 / 06期

关键词：

D O I：

10.1007/s11906-004-0035-3

中图分类号：

R6 [外科学];

学科分类号：

1002 [临床医学]; 100210 [外科学];

摘要：

Diabetes results in a cardiomyopathy characterized by reduced contractility that is primarily the result of changes in calcium handling within the myocyte. Because most of the calcium involved in excitation-contraction (EC) coupling is derived from the sarcoplasmic reticulum (SR), it is no surprise that many studies have found a reduction in sarcoendoplasmic reticulum calcium ATPase (SERCA) activity in the diabetic state. In this review, we outline the changes to A calcium handling in the diabetic state and, through the use of transgenic mice and adenoviral gene therapy, we examine how SR function can be improved by the expression of various proteins that are directly and indirectly involved in calcium handling. Improving SERCA activity plays an important role in ameliorating the contractile phenotype associated with the diabetic state.

引用

页码：424 / 429

页数：6

共 52 条

[1]

Age-dependent changes in metabolism, contractile function, and ischemic sensitivity in hearts from db/db mice [J].

Aasum, E ;

Hafstad, AD ;

Severson, DL ;

Larsen, TS .

DIABETES, 2003, 52 (02) :434-441

[2]

Enhanced inhibition of L-type calcium currents by troglitazone in streptozotocin-induced diabetic rat cardiac ventricular myocytes [J].

Arikawa, M ;

Takahashi, N ;

Kira, T ;

Hara, M ;

Saikawa, T ;

Sakata, T .

BRITISH JOURNAL OF PHARMACOLOGY, 2002, 136 (06) :803-810

[3]

BETA-ADRENERGIC RECEPTORS, ADENYLATE-CYCLASE ACTIVITY, AND CARDIAC DYSFUNCTION IN THE DIABETIC RAT [J].

ATKINS, FL ;

DOWELL, RT ;

LOVE, S .

JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 1985, 7 (01) :66-70

[4]

Multiple Sp1 binding sites in the cardiac slow twitch muscle sarcoplamsic reticulum Ca2+-ATPase gene promoter are required for expression in Sol8 muscle cells [J].

Baker, DL ;

Dave, V ;

Reed, T ;

Periasamy, M .

JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (10) :5921-5928

[5]

Insulin signaling coordinately regulates cardiac size, metabolism, and contractile protein isoform expression [J].

Belke, DD ;

Betuing, S ;

Tuttle, MJ ;

Graveleau, C ;

Young, ME ;

Pham, M ;

Zhang, DF ;

Cooksey, RC ;

McClain, DA ;

Litwin, SE ;

Taegtmeyer, H ;

Severson, D ;

Kahn, CR ;

Abel, ED .

JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (05) :629-639

[6]

Diabetes increases formation of advanced glycation end products on sarco(endo)plasmic reticulum Ca2+-ATPase [J].

Bidasee, KR ;

Zhang, YN ;

Shao, CH ;

Wang, M ;

Patel, KP ;

Dincer, ÜD ;

Besch, HR .

DIABETES, 2004, 53 (02) :463-473

[7]

Chronic diabetes increases advanced glycation end products on cardiac ryanodine receptors/calcium release channels [J].

Bidasee, KR ;

Nallani, K ;

Yu, YQ ;

Cocklin, RR ;

Zhang, YN ;

Wang, M ;

Dincer, ÜD ;

Besch, HR .

DIABETES, 2003, 52 (07) :1825-1836

[8]

BOUCHARD RA, AM J PHYSL, V160, pH341

[9]

Maximal inhibition of SERCA2 Ca2+ affinity by phospholamban in transgenic hearts overexpressing a non-phosphorylatable form of phospholamban [J].

Brittsan, AG ;

Carr, AN ;

Schmidt, AG ;

Kranias, EG .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (16) :12129-12135

[10]

The effect of isoproterenol on phospholamban-deficient mouse hearts with altered thyroid conditions [J].

Brittsan, AG ;

Kiss, E ;

Edes, I ;

Grupp, IL ;

Grupp, G ;

Kranias, EG .

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 1999, 31 (09) :1725-1737

← 1 2 3 4 5 6 →