Advances in Cardiology最新文献

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Role of connexin43-interacting proteins at gap junctions. 连接蛋白43相互作用蛋白在间隙连接中的作用。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092561
Ben N G Giepmans
{"title":"Role of connexin43-interacting proteins at gap junctions.","authors":"Ben N G Giepmans","doi":"10.1159/000092561","DOIUrl":"https://doi.org/10.1159/000092561","url":null,"abstract":"<p><p>Gap junctions are arrays of cell-to-cell channels that allow diffusion of small molecules between neighboring cells. The individual channels are formed by the four-transmembrane connexin (Cx) proteins. Recently, multiple proteins have been found to interact at the cytoplasmic site with the most abundant connexin, Cx43, but physiological data about the role of these interactions is scarce. Here, molecular detail about Cx43 interactions is presented and the putative roles of Cx43-interacting proteins are discussed. Emphasis is on new insights into the interactions of c-Src and ZO-1 with Cx43, interacting proteins discovered within the last 2 years (drebrin, CIP85, CCN3), and feedback between gap junctions, adherens junctions (N-cadherin and catenins) and the cytoskeleton (microtubules and actin).</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"41-56"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092561","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26434949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 99
Life cycle of connexins: regulation of connexin synthesis and degradation. 连接蛋白的生命周期:连接蛋白合成和降解的调控。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092562
Aida Salameh
{"title":"Life cycle of connexins: regulation of connexin synthesis and degradation.","authors":"Aida Salameh","doi":"10.1159/000092562","DOIUrl":"https://doi.org/10.1159/000092562","url":null,"abstract":"<p><p>Gap-junction-forming connexins (Cx) exhibit a complex life cycle which is regulated at various levels. First, the promoter regions and binding of transcription factors to them control the transcription of the connexin genes. Translation of Cx-mRNA seems to be enabled by internal ribosome entry site elements allowing translation even under stress conditions. The newly synthetized Cx protein (monomeric) is transferred to the Golgi apparatus, oligomerized, transferred to the plasma membrane and incorporated into gap junction plaques. Two principal pathways for degradation of Cx could be defined: (a) lysosomal and (b) proteasomal degradation, including phosphorylation and ubiquitination as well as the internalization of complete gap junction channels as annular gap junctions doomed to degradation. In the present article, the various steps of the life cycle of cardiac connexins and its regulation are reviewed.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"57-70"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092562","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26434950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 37
Clinical perspectives of heart rate slowing for coronary event reduction and heart failure. 心率减慢对减少冠状动脉事件和心力衰竭的临床意义。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000095405
Nicolas Danchin, Zena Kadri
{"title":"Clinical perspectives of heart rate slowing for coronary event reduction and heart failure.","authors":"Nicolas Danchin,&nbsp;Zena Kadri","doi":"10.1159/000095405","DOIUrl":"https://doi.org/10.1159/000095405","url":null,"abstract":"<p><p>Heart rate is a major determinant of myocardial oxygen consumption. There is ample evidence of an association between high heart rate and poor outcome in numerous clinical settings. Experimental studies in monkeys have shown a link between increased heart rate and development of atherosclerosis. In the clinical setting, increased heart rate has been found associated with coronary plaque rupture. A causal relationship is further supported by the fact that Beta-blockers have a well-documented efficacy after myocardial infarction, although the other properties of these agents may also participate in their protective effect. Beyond the potential benefits of heart rate lowering in patients with coronary artery disease, medications capable of decreasing heart rate without altering left ventricular function, such as the I(f) current inhibitor ivabradine, might prove particularly helpful in patients with chronic heart failure associated with coronary artery disease, but also in heart failure without systolic dysfunction, or in patients needing inotropic support for acute heart failure.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"43 ","pages":"45-53"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000095405","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26224070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 3
Heart rate: a risk factor for cardiac diseases and outcomes? Pathophysiology of cardiac diseases and the potential role of heart rate slowing. 心率:心脏病及其后果的危险因素?心脏疾病的病理生理学和心率减慢的潜在作用。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000095401
Gaetano Antonio Lanza, Kim Fox, Filippo Crea
{"title":"Heart rate: a risk factor for cardiac diseases and outcomes? Pathophysiology of cardiac diseases and the potential role of heart rate slowing.","authors":"Gaetano Antonio Lanza,&nbsp;Kim Fox,&nbsp;Filippo Crea","doi":"10.1159/000095401","DOIUrl":"https://doi.org/10.1159/000095401","url":null,"abstract":"<p><p>Several cohort studies have shown that increasing heart rate (HR) is a predictor of cardiovascular mortality in apparently healthy subjects, independent of several other potential coronary risk factors. Increased resting HR is also a well-known negative prognostic sign in patients with acute myocardial infarction (MI) and in those with heart failure. The predictive value of HR in MI patients extends at long-term follow-up, is independent of most clinical parameters, including left ventricular function, and seems maintained in the modern era of aggressive reperfusion treatment. In accordance with these data, numerous clinical studies have demonstrated that Beta-blockade, which decreases HR, has significant favorable clinical effects in patients with a history of acute MI or heart failure. Although the unfavorable prognostic effect of HR may reflect the deleterious effect of a sympathovagal imbalance, characterized by sympathetic predominance and vagal depression, several data suggest that HR may by itself cause negative effects on cardiovascular function, inducing an increase in cardiac work and myocardial oxygen consumption and a reduction of the diastolic time, with a reduction of time of myocardial blood supply, both conditions favoring the development of myocardial ischemia, besides facilitating arrhythmias in myocardial ischemic areas, by reentry mechanisms. Thus, a reduction of HR might have direct beneficial clinical effects, as also suggested by experimental findings.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"43 ","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000095401","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26224067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 39
Heart rate reduction by pharmacological If current inhibition. 通过药物电流抑制降低心率。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000095404
A Cargnoni, C Ceconi, G Stavroula, R Ferrari
{"title":"Heart rate reduction by pharmacological If current inhibition.","authors":"A Cargnoni,&nbsp;C Ceconi,&nbsp;G Stavroula,&nbsp;R Ferrari","doi":"10.1159/000095404","DOIUrl":"https://doi.org/10.1159/000095404","url":null,"abstract":"<p><p>Heart rate reduction is becoming a new strategy to treat coronary patients. The development of heart-rate-lowering drugs, with a more specific activity than Beta-blockers, coincides with the detection of the sinoatrial pacemaker I(f) current. The first selective I(f) inhibitor that has been approved for clinical use is ivabradine. Ivabradine has been shown to reduce heart rate, preserve myocardial contractility, increase diastolic filling and maintain both small and large coronary artery vasodilation, whatever the level of exercise, thus ensuring adequate endocardial blood perfusion during exercise. Furthermore ivabradine decreases myocardial oxygen consumption and improves myocardial energetics, protecting the myocardium during acute ischemic conditions and showing favorable antiremodelling properties in patients with chronic ischemic disease.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"43 ","pages":"31-44"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000095404","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26224069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 11
Connexins in atherosclerosis. 动脉粥样硬化中的连接蛋白。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092574
Christos E Chadjichristos, Jean-Paul Derouette, Brenda R Kwak
{"title":"Connexins in atherosclerosis.","authors":"Christos E Chadjichristos, Jean-Paul Derouette, Brenda R Kwak","doi":"10.1159/000092574","DOIUrl":"10.1159/000092574","url":null,"abstract":"<p><p>Remodeling of the vascular wall plays a central role in many physiological processes, but also in the pathogenesis of cardiovascular diseases such as atherosclerosis and restenosis. Atherosclerosis represents the major cause of death and disability in adult populations of Western societies. Angioplasty is a common and effective method of treatment for coronary atherosclerosis, but restenosis after the procedure continues to be a serious clinical complication. The development of atherosclerosis and restenosis involves complex patterns of interactions between the dysfunctional endothelium, inflammatory cells and smooth muscle cells in which cytokines and growth factors are known to play a critical role. Apart from paracrine cell-to-cell signaling, a role for gap-junction-mediated intercellular communication has recently been suggested. In this chapter, we summarize existing evidence supporting such a role. Thus, the pattern of vascular connexins is altered during atherosclerotic plaque formation and in restenosis. In addition, disturbances in flow, inflammation and smooth muscle cell activation and proliferation have been shown to affect connexin expression or gap junctional communication. Finally, genetically modified connexin expression alters the course of these diseases in mice. Further studies will tell us whether future treatment of atherosclerosis or restenosis may involve connexin-based strategies.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"255-267"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092574","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26376462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 25
Connexin-dependent communication within the vascular wall: contribution to the control of arteriolar diameter. 血管壁内连接蛋白依赖的通讯:对小动脉直径控制的贡献。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092575
Cor de Wit, Stephanie E Wölfle, Bernd Höpfl
{"title":"Connexin-dependent communication within the vascular wall: contribution to the control of arteriolar diameter.","authors":"Cor de Wit,&nbsp;Stephanie E Wölfle,&nbsp;Bernd Höpfl","doi":"10.1159/000092575","DOIUrl":"https://doi.org/10.1159/000092575","url":null,"abstract":"<p><p>Communication between cells is important to the microcirculation and enables the coordination of cellular behavior along the length of the vessel. Arterioles span considerable distances within the microcirculatory network, and thus flow changes require the adaptation of vessel resistance over the whole length of the vessel in order to be effective. Such a task requires communication along the vessel wall, and gap junction channels that connect endothelial as well as smooth muscle cells with each other set the stage for this requirement. Communication along the vessel wall can be tested experimentally by confined local stimulation of arterioles either in vitro or in vivo. Certain vascular stimuli induce both a local response and a concomitant uniform remote response, confirming the rapid conduction of vasomotor stimuli along the vessel wall. Gap junctions in vascular tissue are composed of connexins (Cx) Cx40, Cx43, Cx37 and Cx45. Of these, Cx40 is of special importance: its lack results in a deficient conduction of vasodilator stimuli along the vessel wall. Interestingly, Cx40-deficient mice display an elevated mean arterial pressure, suggesting that Cx40-depending gap junctional coupling is necessary to regulate vascular behavior and peripheral resistance. While the role of other connexins is less well established, an abundance of experimental data has proven the necessity of gap junctional communication to coordinate vascular behavior during adaptive blood flow regulation.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"268-283"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092575","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26376463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 53
Connexins and cardiac arrhythmias. 连接素和心律失常。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092567
Harold V M van Rijen, Toon A B van Veen, Daniel Gros, Ronald Wilders, Jacques M T de Bakker
{"title":"Connexins and cardiac arrhythmias.","authors":"Harold V M van Rijen,&nbsp;Toon A B van Veen,&nbsp;Daniel Gros,&nbsp;Ronald Wilders,&nbsp;Jacques M T de Bakker","doi":"10.1159/000092567","DOIUrl":"https://doi.org/10.1159/000092567","url":null,"abstract":"<p><p>During cardiac remodeling, impulse conduction in the heart is altered by changes in excitability, electrical coupling, and tissue architecture. The impairment of normal impulse conduction is one of the factors that increases the propensity for arrhythmias. This chapter focuses on the relationship between electrical coupling between ventricular myocytes and arrhythmogenesis. Mouse models of decreased electrical coupling in the heart have shown that a clinically relevant 50% reduction in gap junctions in the heart has no effect on impulse conduction or arrhythmogenesis. To impair conduction and arrhythmias, coupling has to be reduced to very low levels. Apparently, there is a large conduction reserve, which can preserve normal impulse conduction even when electrical coupling is moderately reduced. However, cardiac remodeling is also associated with reduced excitability and increased levels of collagen deposition (fibrosis). It is therefore presumably the combination of, in itself ineffective, reduction of electrical coupling with other impairments like fibrosis or reduced excitability that causes the limits of conduction reserve to be exceeded, thereby resulting in abnormal impulse conduction and enhanced arrhythmogenesis.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"150-160"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092567","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26377039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 57
Connexins in the sinoatrial and atrioventricular nodes. 中房和房室结中的连接蛋白
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000092569
M R Boyett, S Inada, S Yoo, J Li, J Liu, J Tellez, I D Greener, H Honjo, R Billeter, M Lei, H Zhang, I R Efimov, H Dobrzynski
{"title":"Connexins in the sinoatrial and atrioventricular nodes.","authors":"M R Boyett, S Inada, S Yoo, J Li, J Liu, J Tellez, I D Greener, H Honjo, R Billeter, M Lei, H Zhang, I R Efimov, H Dobrzynski","doi":"10.1159/000092569","DOIUrl":"10.1159/000092569","url":null,"abstract":"<p><p>The sinoatrial node (SAN) and the atrioventricular node (AVN) are specialized tissues in the heart: the SAN is specialized for pacemaking (it is the pacemaker of the heart), whereas the AVN is specialized for slow conduction of the action potential (to introduce a delay between atrial and ventricular activation during the cardiac cycle). These functions have special requirements regarding electrical coupling and, therefore, expression of connexin isoforms. Electrical coupling in the center of the SAN should be weak to protect it from the inhibitory electrotonic influence of the more hyperpolarized non-pacemaking atrial muscle surrounding the SAN. However, for the SAN to be able to drive the atrial muscle, electrical coupling should be strong in the periphery of the SAN. Consistent with this, in the center of the SAN there is no expression of Cx43 (the principal connexin of the working myocardium) and little expression of Cx40, but there is expression of Cx45 and Cx30.2, whereas in the periphery of the SAN Cx43 as well Cx45 is expressed. In the AVN, there is a similar pattern of expression of connexins as in the center of the SAN and this is likely to be in large part responsible for the slow conduction of the action potential.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"42 ","pages":"175-197"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000092569","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26377041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 131
Heart rate slowing versus other pharmacological antianginal strategies. 心率减慢与其他药物抗心绞痛策略。
Advances in Cardiology Pub Date : 2006-01-01 DOI: 10.1159/000095429
Ariel Diaz, Jean-Claude Tardif
{"title":"Heart rate slowing versus other pharmacological antianginal strategies.","authors":"Ariel Diaz,&nbsp;Jean-Claude Tardif","doi":"10.1159/000095429","DOIUrl":"https://doi.org/10.1159/000095429","url":null,"abstract":"<p><p>Relieving the symptoms of angina and improving the quality of life and functional status are important objectives in the management of patients with chronic stable angina. A high heart rate induces or exacerbates myocardial ischemia and angina because it both increases oxygen demand and decreases myocardial perfusion. Beta-Blockers are effective at reducing anginal symptoms largely by decreasing heart rate. Physician use and patient compliance may be limited by the side effects of Beta-blockers which include fatigue, depression and sexual dysfunction. Heart rate reduction can also be obtained by the calcium antagonists verapamil and diltiazem and by the new selective heart-rate-reducing agent ivabradine. Ivabradine (Procoralan) is a selective and specific I(f) inhibitor that acts on one of the most important ionic currents for the regulation of the pacemaker activity of sinoatrial node cells. Ivabradine has demonstrated dosedependent anti-ischemic and antianginal effects in a placebo-controlled study. The INITIATIVE trial is a large multicenter trial in which 939 patients with stable angina were randomized to ivabradine or atenolol. The noninferiority of ivabradine was shown in the INITIATIVE trial at all doses and for all criteria including time to limiting angina. The number of angina attacks per week was decreased by two thirds with both ivabradine and atenolol. In another trial of 1,195 patients, time to 1mm ST segment depression was increased by 45 s with ivabradine 7.5 mg b.i.d. and by 40 s with amlodipine 10 mg daily. Unlike beta-blockers, ivabradine is devoid of intrinsic negative inotropic effects and does not affect coronary vasomotion. A whole range of patients with angina may benefit from exclusive heart rate reduction with ivabradine, including those with contraindications or intolerance to the use of beta-blockers and patients that are insufficiently controlled by beta-blockers or calcium channel blockers.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"43 ","pages":"65-78"},"PeriodicalIF":0.0,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000095429","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26224072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 7
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