Journal of Molecular and Cellular Cardiology (J MOL CELL CARDIOL)

Publisher: International Society for Heart Research, Elsevier

Journal description

The Journal of Molecular and Cellular Cardiology, the official organ of the International Society for Heart Research, provides a forum for research papers dealing with the molecular biology, physiology, pharmacology, and pathophysiology of the heart and c

Current impact factor: 4.66

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 4.655
2013 Impact Factor 5.218
2012 Impact Factor 5.148
2011 Impact Factor 5.166
2010 Impact Factor 5.499
2009 Impact Factor 4.965
2008 Impact Factor 5.054
2006 Impact Factor 4.859
2005 Impact Factor 3.872
2004 Impact Factor 4.198
2003 Impact Factor 4.954
2002 Impact Factor 4.091
2001 Impact Factor 3.396
2000 Impact Factor 3.383
1999 Impact Factor 2.923
1998 Impact Factor 2.72
1997 Impact Factor 3.255
1996 Impact Factor 2.742
1995 Impact Factor 2.78
1994 Impact Factor 3.008
1993 Impact Factor 3.485
1992 Impact Factor 3.115

Impact factor over time

Impact factor
Year

Additional details

5-year impact 5.04
Cited half-life 6.30
Immediacy index 1.17
Eigenfactor 0.03
Article influence 1.57
Website Journal of Molecular and Cellular Cardiology website
Other titles Journal of molecular and cellular cardiology (Online), Journal of molecular and cellular cardiology
ISSN 0022-2828
OCLC 36945690
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification
    green

Publications in this journal

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    [Show abstract] [Hide abstract]
    ABSTRACT: The adult human myocardium is incapable of regeneration; yet, the zebrafish (Danio rerio) can regenerate damaged myocardium. Similar to the zebrafish heart, hearts of neonatal, but not adult mice are capable of myocardial regeneration. We performed a proteomics analysis of adult zebrafish hearts and compared their protein expression profile to hearts from neonatal and adult mice. Using two-dimensional difference in-gel electrophoresis (DIGE), there was little overlap between the proteome from adult mouse (8weeks old) and adult zebrafish (18months old) hearts. Similarly, there was a significant degree of mismatch between the protein expression in neonatal and adult mouse hearts. Enrichment analysis of the selected proteins revealed over-expression of DNA synthesis-related proteins in the cardiac proteome of the adult zebrafish heart similar to neonatal and 4days old mice, whereas in hearts of adult mice there was a mitochondria-related predominance in protein expression. Importantly, we noted pronounced differences in the myofilament composition: the adult zebrafish heart lacks many of the myofilament proteins of differentiated adult cardiomyocytes such as the ventricular isoforms of myosin light chains and nebulette. Instead, troponin I and myozenin 1 were expressed as skeletal isoforms rather than cardiac isoforms. Our proteomics assessment of zebrafish and mammalian hearts challenges the assertions on the translational potential of cardiac regeneration in the zebrafish model. The immature myofilament composition of the fish heart may explain why adult mouse and human cardiomyocytes lack this endogenous repair mechanism.
    Full-text · Article · Jan 2016 · Journal of Molecular and Cellular Cardiology
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    ABSTRACT: In order to maintain an efficient, energy-producing network in the heart, dysfunctional mitochondria are cleared through the mechanism of autophagy, which is closely linked with mitochondrial biogenesis; these, together with fusion and fission comprise a crucial process known as mitochondrial turnover. Until recently, the lack of molecular tools and methods available to researchers has impeded in vivo investigations of turnover. To investigate the process at the level of a single mitochondrion, our laboratory has developed the MitoTimer protein. Timer is a mutant of DsRed fluorescent protein characterized by transition from green fluorescence to a more stable red conformation over 48 h, and its rate of maturation is stable under physiological conditions. We fused the Timer cDNA with the inner mitochondrial membrane signal sequence and placed it under the control of a cardiac-restricted promoter. This construct was used to create the alpha-MHC-MitoTimer mice. Surprisingly, initial analysis of the hearts from these mice demonstrated a high degree of heterogeneity in the ratio of red-to-green fluorescence of MitoTimer in cardiac tissue. Further, scattered solitary mitochondria within cardiomyocytes display a much higher red-to-green fluorescence (red-shifted) relative to other mitochondria in the cell, implying a block in import of newly synthesized MitoTimer likely due to lower membrane potential. These red-shifted mitochondria may represent older, senescent mitochondria. Concurrently, the cardiomyocytes also contain a subpopulation of mitochondria that display a lower red-to-green fluorescence (green-shifted) relative to other mitochondria, indicative of germinal mitochondria that are actively engaged in import of newly-synthesized mito-targeted proteins. These mitochondria can be isolated and sorted from the heart by flow cytometry for further analysis. Initial studies suggest that these mice represent an elegant tool for the investigation of mitochondrial turnover in the heart.
    Preview · Article · Dec 2015 · Journal of Molecular and Cellular Cardiology

  • No preview · Article · Sep 2015 · Journal of Molecular and Cellular Cardiology
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    ABSTRACT: Langendorff-perfusion of hearts isolated from rats and mice has been used extensively for physiological, pharmacological and biochemical studies. The ability to reliably phenotype these hearts is, therefore, essential. One of the commonly used indices of function is rate-pressure product (RPP) - a rather ill-defined index of 'work' or, more correctly, 'effort'. RPP, as originally described in dog or human hearts, was shown to correlate with oxygen consumption (MVO2 ). Despite its widespread use, the application of this index to rat or mouse hearts (which, unlike the dog or human, have a negative force-frequency relationship), has not been characterised. The aim of this study was to examine the relationship between RPP and MVO2 in Langendorff rat hearts. Paced hearts (300-750 bpm) were perfused either with Krebs-Henseleit buffer (KH, 11 mm glucose) or buffer supplemented with metabolic substrates and insulin. A-V oxygen consumption (MVO2 ) was recorded. Metabolic status was assessed using (31) P MR Spectroscopy and lactate efflux. Experiments were repeated in the presence of isoprenaline (ISO) and in unpaced hearts where heart rate was increased by cumulative ISO challenge. In KH- perfused hearts, MVO2 increased with increasing heart rate but as LVDP declined with increases in rate, RPP did not correlate with MVO2 , lactate production or PCr/ATP ratio. While the provision of substrates or β-stimulation changed the shape of the RPP-MVO2 relationship, neither intervention resulted in a positive correlation between RPP and oxygen consumption. RPP is therefore an unreliable index of oxygen consumption or 'cardiac effort' in the isolated rat heart. This article is protected by copyright. All rights reserved.
    No preview · Article · Sep 2015 · Journal of Molecular and Cellular Cardiology

  • No preview · Article · Sep 2015 · Journal of Molecular and Cellular Cardiology
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    ABSTRACT: The estrogen-mediated vasculoprotective effect has been widely reported in many animal studies, although the clinical trials are controversial and the detailed mechanisms remain unclear. In this study, we focused on the molecular mechanism and consequence of 17β-estradiol (E2)-induced ERRα (estrogen-related receptor alpha) expression in endothelium and its potential beneficial effects on vascular function. The human aorta endothelial cells were used to identify the detailed molecular mechanism and consequences for E2-induced ERRα expression through estrogen receptors (ER), where ERα responses E2-induced ERRα activation, and ERβ responses basal ERRα expression. E2-induced ERRα expression increases fatty acid uptake/oxidation with increased mitochondrial replication, ATP generation and attenuated reactive oxygen species (ROS) formation. We have obtained further in vivo proof from high-fat diet mice that the lentivirus-carried endothelium-specific delivery of ERRα expression on the vascular wall normalizes E2 deficiency-induced increased plasma lipids with ameliorated vascular damage. ERRα knockdown worsens the problem, and the E2 could only partly restore this effect. This is the first time we report the detailed mechanism with direct evidence that E2-induced ERRα expression modulates the fatty acid metabolism and reduces the circulating lipids through endothelium. We conclude that E2-induced ERRα expression in endothelium plays an important role for the E2-induced vasculoprotective effect. Copyright © 2015. Published by Elsevier Ltd.
    No preview · Article · Aug 2015 · Journal of Molecular and Cellular Cardiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: The estrogen-mediated vasculoprotective effect has been widely reported in many animal studies, although the clinical trials are controversial and the detailed mechanisms remain unclear. In this study, we focused on the molecular mechanism and consequence of 17β-estradiol (E2)-induced ERRα (estrogen-related receptor alpha) expression in endothelium and its potential beneficial effects on vascular function. The human aorta endothelial cells were used to identify the detailed molecular mechanism and consequences for E2-induced ERRα expression through estrogen receptors (ER), where ERα responses E2-induced ERRα activation, and ERβ responses basal ERRα expression. E2-induced ERRα expression increases fatty acid uptake/oxidation with increased mitochondrial replication, ATP generation and attenuated reactive oxygen species (ROS) formation. We have obtained further in vivo proof from high-fat diet mice that the lentivirus-carried endothelium-specific delivery of ERRα expression on the vascular wall normalizes E2 deficiency-induced increased plasma lipids with ameliorated vascular damage. ERRα knockdown worsens the problem, and the E2 could only partly restore this effect. This is the first time we report the detailed mechanism with direct evidence that E2-induced ERRα expression modulates the fatty acid metabolism and reduces the circulating lipids through endothelium. We conclude that E2-induced ERRα expression in endothelium plays an important role for the E2-induced vasculoprotective effect.
    No preview · Article · Aug 2015 · Journal of Molecular and Cellular Cardiology
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    ABSTRACT: BACKGROUND: Cardiac alternans are proarrhythmic and mechanistically link cardiac mechanical dysfunction and sudden cardiac death. Beat-to-beat alternans occur when beats with large Ca2+ transients and long action potential duration (APD) alternate with the converse. APD alternans are typically driven by Ca2+ alternans and sarcoplasmic reticulum (SR) Ca2+ release alternans. But the effect of intercellular communication via gap junctions (GJ) on alternans in intact heart remains unknown. OBJECTIVE: We assessed the effects of cell-to-cell coupling on local alternans in intact Langendorff-perfused mouse hearts, measuring single myocyte [Ca2+] alternans synchronization among neighboring cells, and effects of β-adrenergic receptor (β-AR) activation and reduced GJ coupling. METHODS AND RESULTS: Mouse hearts (C57BL/6) were retrogradely perfused and loaded with Fluo-8 AM to record cardiac myocyte [Ca2+] in situ with confocal microscopy. Single cell resolution allowed analysis of alternans within the intact organ during alternans induction. Carbenoxolone (25 μM), a GJ inhibitor, significantly increased the occurrence and amplitude of alternans in single cells within the intact heart. Alternans were concordant between neighboring cells throughout the field of view, except transiently during onset. β-AR stimulation only reduced Ca2+ alternans in tissue that had reduced GJ coupling, matching effects seen in isolated myocytes. CONCLUSIONS: Ca2+ alternans among neighboring myocytes is predominantly concordant, likely because of electrical coupling between cells. Consistent with this, partial GJ uncoupling increased propensity and amplitude of Ca2+ alternans, and made them more sensitive to reversal by β-AR activation, as in isolated myocytes. Electrical coupling between myocytes may thus limit the alternans initiation, but also allow alternans to be more stable once established.
    No preview · Article · Mar 2015 · Journal of Molecular and Cellular Cardiology
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    Preview · Article · Mar 2015 · Journal of Molecular and Cellular Cardiology