AMP-Activated protein kinase: A key stress signaling pathway in the heart

被引：138

作者：

Young, LH ^{[1
]}

Li, J ^{[1
]}

Baron, SJ ^{[1
]}

Russell, RR ^{[1
]}

机构：

[1] Yale Univ, Sch Med, Dept Internal Med, Sect Cardiovasc Med, New Haven, CT 06510 USA

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2005年 / 15卷 / 03期

关键词：

D O I：

10.1016/j.tcm.2005.04.005

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

AMP-activated protein kinase (AMPK) is activated during exercise and ischemia and is emerging as an important regulatory mechanism in the heart. AMPK promotes adenosine triphosphate-generating pathways, including glucose transport, glycolysis, and fatty acid oxidation, while inhibiting energy-consuming anabolic pathways. After ischemia-reperfusion, AMPK-deficient hearts from transgenic mice have severe left ventricular contractile dysfunction with increased apoptosis and necrosis. Mutations in the AMPK gamma(2) subunit lead to cardiac glycogen overload, Wolff-Parkinson-White syndrome, arrhythmias, and heart failure. This review focuses on the molecular mechanisms of activation and cardiovascular actions of AMPK in the heart.

引用

页码：110 / 118

页数：9

共 89 条

[1] Myocardial ischemia differentially regulates LKB1 and an alternate 5′-AMP-activated protein kinase kinase [J].

Altarejos, JY ;

Taniguchi, M ;

Clanachan, AS ;

Lopaschuk, GD .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2005, 280 (01) :183-190

[2]

Andersson L, 2003, BIOCHEM SOC T, V31, P232, DOI 10.1042/BST0310232

[3] AMP-activated protein kinase plays a role in the control of food intake [J].

Andersson, U ;

Filipsson, K ;

Abbott, CR ;

Woods, A ;

Smith, K ;

Bloom, SR ;

Carling, D ;

Small, CJ .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (13) :12005-12008

[4] Transgenic mice overexpressing mutant PRKAG2 define the cause of Wolff-Parkinson-White syndrome in glycogen storage cardiomyopathy [J].

Arad, M ;

Moskowitz, IP ;

Patel, VV ;

Ahmad, F ;

Perez-Atayde, AR ;

Sawyer, DB ;

Walter, M ;

Li, GH ;

Burgon, PG ;

Maguire, CT ;

Stapleton, D ;

Schmitt, JP ;

Guo, XX ;

Pizard, A ;

Kupershmidt, S ;

Roden, DM ;

Berul, CI ;

Seidman, CE ;

Seidman, JG .

CIRCULATION, 2003, 107 (22) :2850-2856

[5] Constitutively active AMP kinase mutations cause glycogen storage disease mimicking hypertrophic cardiomyopathy [J].

Arad, M ;

Benson, DW ;

Perez-Atayde, AR ;

McKenna, WJ ;

Sparks, EA ;

Kanter, RJ ;

McGarry, K ;

Seidman, JG ;

Seidman, CE .

JOURNAL OF CLINICAL INVESTIGATION, 2002, 109 (03) :357-362

[6] Dual mechanisms regulating AMPK kinase action in the ischemic heart [J].

Baron, SJ ;

Li, J ;

Russell, RR ;

Neumann, D ;

Miller, EJ ;

Tuerk, R ;

Wallimann, T ;

Hurley, RL ;

Witters, LA ;

Young, LH .

CIRCULATION RESEARCH, 2005, 96 (03) :337-345

[7] Glucose metabolism in perfused mouse hearts overexpressing human GLUT-4 glucose transporter [J].

Belke, DD ;

Larsen, TS ;

Gibbs, EM ;

Severson, DL .

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2001, 280 (03) :E420-E427

[8] Effect of AMPK activation on muscle glucose metabolism in conscious rats [J].

Bergeron, R ;

Russell, RR ;

Young, LH ;

Ren, JM ;

Marcucci, M ;

Lee, A ;

Shulman, GI .

AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 1999, 276 (05) :E938-E944

[9] Mutations in the γ2 subunit of AMP-activated protein kinase cause familial hypertrophic cardiomyopathy:: evidence for the central role of energy compromise in disease pathogenesis [J].

Blair, E ;

Redwood, C ;

Ashrafian, H ;

Oliveira, M ;

Broxholme, J ;

Kerr, B ;

Salmon, A ;

Östman-Smith, I ;

Watkins, H .

HUMAN MOLECULAR GENETICS, 2001, 10 (11) :1215-1220

[10] Uncoupling proteins 2 and 3 - Potential regulators of mitochondrial energy metabolism [J].

Boss, O ;

Hagen, T ;

Lowell, BB .

DIABETES, 2000, 49 (02) :143-156

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