Alteration of the Beta-Adrenergic Signaling Pathway in Human Heart Failure

被引：1

作者：

Hamdani, Nazha ^{[1
]}

Linke, Wolfgang A. ^{[1
]}

机构：

[1] Ruhr Univ Bochum, Dept Cardiovasc Physiol, Inst Physiol, D-44780 Bochum, Germany

来源：

CURRENT PHARMACEUTICAL BIOTECHNOLOGY | 2012年 / 13卷 / 13期

关键词：

Heart failure; beta adrenergic receptors; myofilament proteins; cardiomyocytes; PROTEIN-KINASE-C; CARDIAC TROPONIN-I; MYOSIN HEAVY-CHAIN; LEFT-VENTRICULAR FUNCTION; RECEPTOR MESSENGER-RNA; T ISOFORM EXPRESSION; SARCOPLASMIC-RETICULUM; PASSIVE STIFFNESS; DOWN-REGULATION; IMMUNOELECTRON MICROSCOPY;

D O I：

暂无

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：

Heart failure is characterized by elevated circulating catecholamine levels and extensive abnormalities in beta-adrenergic receptor signaling. Under physiological conditions, sympathetic modulation via catecholamines induces positive inotropic, chronotropic and lusitropic responses. Well established in heart failure patients is a pronounced activation of the sympathetic system, accompanied by downregulation and desensitization of beta-adrenergic receptors, leading to a markedly diminished beta-adrenergic contractile response. In this review, we will discuss the normal beta-adrenergic receptor signaling pathway in the heart and focus on the pathphysiological alterations of beta-adrenergic receptor signaling and contractile proteins in heart failure.

引用

页码：2522 / 2531

页数：10

共 124 条

[1]

ANDERSON PAW, 1992, BASIC RES CARDIOL, V87, P117

[2] TROPONIN-T ISOFORM EXPRESSION IN HUMANS - A COMPARISON AMONG NORMAL AND FAILING ADULT HEART, FETAL HEART, AND ADULT AND FETAL SKELETAL-MUSCLE [J].

ANDERSON, PAW ;

MALOUF, NN ;

OAKELEY, AE ;

PAGANI, ED ;

ALLEN, PD .

CIRCULATION RESEARCH, 1991, 69 (05) :1226-1233

[3] β3-Adrenoceptors modulate left ventricular relaxation in the rat heart via the NO-cGMP-PKG pathway [J].

Angelone, T. ;

Filice, E. ;

Quintieri, A. M. ;

Imbrogno, S. ;

Recchia, A. ;

Pulera, E. ;

Mannarino, C. ;

Pellegrino, D. ;

Cerra, M. C. .

ACTA PHYSIOLOGICA, 2008, 193 (03) :229-239

[4]

[Anonymous], 2001, AM J MED, DOI DOI 10.1016/S0002-9343(98)00385-4

[5] Endothelial dysfunction in patients with heart failure: Relationship to disease severity [J].

Bank, AJ ;

Lee, PC ;

Kubo, SH .

JOURNAL OF CARDIAC FAILURE, 2000, 6 (01) :29-36

[6] Augmented protein kinase C-α-induced myofilament protein phosphorylation contributes to myofilament dysfunction in experimental congestive heart failure [J].

Belin, Rashad J. ;

Sumandea, Marius P. ;

Allen, Edward J. ;

Schoenfelt, Kelly ;

Wang, Helen ;

Solaro, R. John ;

de Tombe, Pieter P. .

CIRCULATION RESEARCH, 2007, 101 (02) :195-204

[7] STRUCTURAL BASIS OF END-STAGE FAILURE IN ISCHEMIC CARDIOMYOPATHY IN HUMANS [J].

BELTRAMI, CA ;

FINATO, N ;

ROCCO, M ;

FERUGLIO, GA ;

PURICELLI, C ;

CIGOLA, E ;

QUAINI, F ;

SONNENBLICK, EH ;

OLIVETTI, G ;

ANVERSA, P .

CIRCULATION, 1994, 89 (01) :151-163

[8] Cardiac excitation-contraction coupling [J].

Bers, DM .

NATURE, 2002, 415 (6868) :198-205

[9] Troponin I phosphorylation in the normal and failing adult human heart [J].

Bodor, GS ;

Oakeley, AE ;

Allen, PD ;

Crimmins, DL ;

Ladenson, JH ;

Anderson, PAW .

CIRCULATION, 1997, 96 (05) :1495-1500

[10] Cardiomyocyte stiffness in Diastolic heart failure [J].

Borbély, A ;

van der Velden, J ;

Papp, Z ;

Bronzwaer, JGF ;

Edes, I ;

Stienen, GJM ;

Paulus, WJ .

CIRCULATION, 2005, 111 (06) :774-781

← 1 2 3 4 5 6 7 8 9 10 →