The role of G protein coupled receptor kinases in neurocardiovascular pathophysiology

被引：12

作者：

Bojic, Tijana ^{[1
]}

Sudar, Emina ^{[1
]}

Mikhailidis, Dimitri ^{[2
]}

Alavantic, Dragan ^{[1
]}

Isenovic, Esma ^{[1
]}

机构：

[1] Univ Belgrade, Lab Radiobiol & Mol Genet, Inst Nucl Sci Vinca, Belgrade 11001, Serbia

[2] UCL, Sch Med, Vasc Dis Prevent Clin, Dept Clin Biochem, London WC1E 6BT, England

来源：

ARCHIVES OF MEDICAL SCIENCE | 2012年 / 8卷 / 06期

关键词：

autonomic; sympathetic; vagal; molecular signaling pathway; BETA-ADRENERGIC RECEPTORS; CHRONIC HEART-FAILURE; MUSCARINIC RECEPTORS; ATRIAL-FIBRILLATION; ORTHOSTATIC HYPOTENSION; BETA-ARK1; INHIBITION; CARDIAC-HYPERTROPHY; VASOVAGAL SYNCOPE; TRANSGENIC MICE; DOWN-REGULATION;

D O I：

10.5114/aoms.2012.29996

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

In coronary artery disease the G protein related kinases (GRKs) play a role in desensitization of beta-adrenoreceptors (AR) after coronary occlusion. Targeted deletion and lowering of cardiac myocyte GRK-2 decreases the risk of post-ischemic heart failure (HF). Studies carried out in humans confirm the role of GRK-2 as a marker for the progression of HF after myocardial infarction (MI). The level of GRK-2 could be an indicator of beta-AR blocker efficacy in patients with acute coronary syndrome. Elevated levels of GRK-2 are an early ubiquitous consequence of myocardial injury. In hypertension an increased level of GRK-2 was reported in both animal models and human studies. The role of GRKs in vagally mediated disorders such as vasovagal syncope and atrial fibrillation remains controversial. The role of GRKs in the pathogenesis of neurocardiological diseases provides an insight into the molecular pathogenesis process, opens potential therapeutic options and suggests new directions for scientific research.

引用

页码：970 / 977

页数：8

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