Current Molecular Medicine (CURR MOL MED)

Publisher: Bentham Science Publishers

Journal description

Current Molecular Medicine is a bimonthly, interdisciplinary journal focused on providing the readership with current and comprehensive reviews on fundamental molecular mechanisms of disease pathogenesis, the development of molecular-diagnosis and/or novel approaches to rational treatment. The reviews should be of significant interest to basic researchers and clinical investigators in molecular medicine. Periodically the journal will invite guest editors to devote an issue on a on a basic research area that shows promise to advance our understanding of the molecular mechanism(s) of a disease or has potential for clinical applications.

Current impact factor: 3.62

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.621
2013 Impact Factor 3.612
2012 Impact Factor 4.197
2011 Impact Factor 4.476
2010 Impact Factor 5.212
2009 Impact Factor 5.096
2008 Impact Factor 5.254
2007 Impact Factor 4.624
2006 Impact Factor 4.85
2005 Impact Factor 4.941

Impact factor over time

Impact factor

Additional details

5-year impact 3.79
Cited half-life 5.50
Immediacy index 0.46
Eigenfactor 0.01
Article influence 1.11
Website Current Molecular Medicine website
Other titles Current molecular medicine (Online)
ISSN 1566-5240
OCLC 55201263
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Bentham Science Publishers

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Author's pre-print on author's personal website, institutional repository and open access repository
    • Author's post-print on author's personal website, institutional repository, open access repository, PubMed Central and arXiv
    • Non-Commercial
    • Published source must be acknowledged
    • Must link to journal homepage with DOI
    • Publisher's version/PDF cannot be used
  • Classification

Publications in this journal

  • No preview · Article · Jan 2016 · Current Molecular Medicine

  • No preview · Article · Nov 2015 · Current Molecular Medicine

  • No preview · Article · Nov 2015 · Current Molecular Medicine
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    ABSTRACT: Angiotensin-converting enzyme inhibitors (ACE-I) improve clinical outcome in patients with myocardial infarction (MI) and chronic heart failure. We investigated potential anti-arrhythmic (AA) benefits in a mouse model of ischemic HF. We hypothesized that normalization of diastolic calcium (Ca2+) by ACE-I may prevent Ca2+-dependent reduction of inward rectifying K+ current (I-K1) and occurrence of arrhythmias after MI. Mice were randomly assigned to three groups: Sham, MI, and MI-D (6 weeks of treatment with ACE-I delapril started 24h after MI). Electrophysiological analyses showed that delapril attenuates MI-induced prolongations of electrocardiogram parameters (QRS complex, QT, QTc intervals) and conduction time from His bundle to ventricular activation. Delapril improved the sympatho-vagal balance (LF/HF) and reduced atrio-ventricular blocks and ventricular arrhythmia. Investigations in cardiomyocytes showed that delapril prevented the decrease of I-K1 measured by patch-clamp technique. I-K1 reduction was related to intracellular Ca2+ overload. This reduction was not observed when intracellular free-Ca2+ was maintained low. Conversely, increasing intracellular free-Ca2+ in Sham following application of SERCA2a inhibitor thapsigargin reduced I-K1. Thapsigargin had no effect in MI animals and abolished the benefits of delapril on I-K1 in MI-D mice. Delapril prevented both the prolongation of action potential late repolarization and the depolarization of resting membrane potential, two phenomena known to trigger abnormal electrical activities, promoted by MI. In conclusion, early chronic therapy with delapril after MI prevented Ca2+-dependent reduction of I-K1. This mechanism may significantly contribute to the antiarrhythmic benefits of ACE-I in patients at risk for sudden cardiac death.
    No preview · Article · Sep 2015 · Current Molecular Medicine

  • No preview · Article · Sep 2015 · Current Molecular Medicine

  • No preview · Article · Aug 2015 · Current Molecular Medicine

  • No preview · Article · Jul 2015 · Current Molecular Medicine
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    ABSTRACT: Tumor-derived autologous antigenic peptides when bound to endogenous 70 kDa family heat shock proteins (HSP70) are able to induce effective T-cell responses against tumors. However, efficacy of HSP-based vaccines in clinical practical stand point still has a number of certain limitations including an activation of immune responses against alien non-human HSPs. In this study we reconstructed the complexes of human recombinant HSPs70 (human recombinant HSP70A1B and HSC70 mixture; hrHSPs70) with antigenic low-weight peptides derived from mice B16F10 melanoma cell lysate (PepMCL) in vitro and investigated the prophylactic potential of these complexes to activate anti-tumor immunity in melanoma mouse model. Our results demonstrate that the developed prophylactic vaccine elicits melanoma-specific immune responses and anti-tumor effects against melanoma. These results suggest that hrHSPs70 has capability to reconstitute complexes with peptides obtained from tumor cells lysates in vitro and, therefore, can be used for delivery of multiple antigenic peptides into antigen-presenting cells (APCs) to activate effectors cells. Designed in such a way hrHSPs70-based prophylactic vaccines induce immune responses resulting in a significant efficient prevention of tumor growth and metastases.
    No preview · Article · Jul 2015 · Current Molecular Medicine

  • No preview · Article · Jun 2015 · Current Molecular Medicine
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    ABSTRACT: FOXQ1 is an oncogene for a variety of tumors and encodes the forkhead boxrelated transcription factor FoxQ1. However, little is known about the role of FoxQ1 in pancreatic cancer (PC). In this study, we examined FoxQ1 expression in PC cell lines and human PC tissues by quantitative PCR and tissue microarray based immunohistochemical staining (IHC), and investigated the clinical correlation between FoxQ1 tissue levels and the clinicopathological characteristics of PC patients. We found that FoxQ1 mRNA expression was up-regulated both in PC cell lines and tumor tissues. IHC results revealed that FoxQ1 was mainly expressed in the cytoplasm, and to a lesser extent in the nucleus of PC cells. FoxQ1 protein levels were significantly higher in PC tissues when compared with matched non-cancerous tissues, and associated positively with the degree of tumor differentiation. Univariate and multivariate survival analysis revealed that patients with high FoxQ1 expression and advanced TNM stage had poor prognosis (HR=1.856, 95%CI 1.065- 3.234, P=0.029; HR=2.091, 95%CI 1.181-3.705, P=0.01). These data indicate that FoxQ1 expression is negatively associated with the overall survival of PC patients, and that this protein may therefore represent a novel molecular target and new prognostic biomarker for PC.
    No preview · Article · Jun 2015 · Current Molecular Medicine
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    ABSTRACT: Human Influenza A virus (IAV), a relatively newer threat to mankind, is becoming invincible due to non availability of proper antiviral drug or effective long lasting vaccine against it. All existing measures to control this virus are overpowered by the phenomena of genetic shift and drift shown by Influenza A virus (IAV). Throughout the world, researchers are exploring the therapeutic potential of antisense technology (AST) to fight against this genetically variable virus. Antisense technology refers to the laboratory manipulation and/or modification of DNA or RNA so that its components (nucleotides) hybridize with target nucleic acid or mRNA or protein itself to inhibit the protein finally encoded. RNA inhibitory (RNAi) mechanism (particularly siRNA) seems to be the most promising among the different agents of AST. However, other agents like oligonucleotides, ribozymes and DNAzymes also show great potential. Decoys and aptamers, alone or in conjunction with other agents, are also being explored to inhibit the replication of virus. Presently, most of these agents have passed initial level of in vitro and in vivo experiments, passing through various levels of clinical trials but none of them has been approved for human purpose till date. Present review consolidates the efforts of researchers worldwide in this particular field and discusses the future perspectives this technology holds, to tame this notorious virus. Day by day, various areas of this technology are being explored and the day is not far when this chemical entity will reach from “bench to bedside”.
    No preview · Article · Jun 2015 · Current Molecular Medicine
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    ABSTRACT: The fact that the phosphatidylinositol 3 kinase (PI3K) signaling pathway is one of the most frequently deregulated signaling networks has triggered intensive efforts in the development of PI3K pathway inhibitors. However, recent clinical trial data have shown only limited activity of PI3K inhibitors at tolerated doses. Thus, there is an urgent need to identify rational combination therapy to improve the efficacy of PI3K-targeted cancer treatment. In this study, we investigated if dietary compound ellagic acid (EA) could improve the therapeutic efficacy of PI3K inhibitor GDC-0941 in breast cancer. Specifically, using a panel of breast cancer cell lines, we showed that combined use of EA and GDC-0941 significantly inhibited cell growth under attached and detached conditions, blocked migration and invasion in vitro as well as tumor initiation and metastasis in vivo. Furthermore, we found that EA promoted apoptosis and further reduced AKT/mTOR activation in GDC-0941- treated breast cancer cells. Together, our data suggest that EA may be a safe and effective agent to boost the efficacy of PI3K-directed breast cancer therapy and that such drug combination may merit further clinical investigation.
    No preview · Article · Jun 2015 · Current Molecular Medicine

  • No preview · Article · May 2015 · Current Molecular Medicine
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    ABSTRACT: Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in adults and its prevalence is rising around the world. This pathology is characterized by accumulation of liver fat, which exceeds 5% of liver weight in absence of alcohol consumption, viral infection or other hepatic etiology. Since NAFLD has been associated with obesity, insulin resistance, diabetes or alteration of lipid profiles, it is considered as the liver manifestation of metabolic syndrome. Pathogenic mechanisms of NAFLD have not been clearly elucidated, but different events such as lipid accumulation, insulin resistance, oxidative and endoplasmic reticulum stress, mitochondrial dysfunction and inflammation are involved. Modifications in lifestyle constitute the first line for the management of NAFLD. Nutritional interventions include low fat and carbohydrate diet with higher polyunsaturated fatty acids ingestion. Moreover, supplementation with antioxidant and cytoprotective agents could be useful to decrease oxidative stress, inflammation and fibrosis. Physical activity enables to reduce the expression of lipogenic genes, fat accumulation, or insulin resistance and improves cardiorespiratory fitness. Benefits have been found following both aerobic exercise and resistance training, and remain even after exercise cessation. However, more studies are required to analyze the molecular and cellular mechanisms involved in nutritional and physical intervention, and to define the volume of activity required and its association with weight loss. In this paper, we offer an updated overview of the mechanisms implicated in the progression of NAFLD, and analyze the beneficial effects of nutritional interventions and physical exercise in the prevention and treatment of this condition.
    No preview · Article · Jan 2015 · Current Molecular Medicine
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    ABSTRACT: HSPB5 or αB-crystallin (αBC) is a major protein of the vertebrate eye lens belonging to the small heat-shock protein family of proteins that respond to various stressful conditions. αBC also is found outside the lens in various non-ocular tissues and acts as a molecular chaperone by preventing aggregation of proteins, inhibits apoptosis and inflammation, and maintains cytoskeletal architecture. The αBC protein is phosphorylated on three serine residues S59, S45, and S19, and several functions of αBC are modulated by phosphorylation. Numerous studies have revealed the upregulation of αBC in pathological conditions such as neurodegenerative diseases, cancers, diabetes, retinal diseases, cataracts, ischemia/repurfusion, aging, and others. However, it is unknown whether the up-regulation of αBC is causative or protective for these pathological conditions. Although αBC has been shown to provide a protective effect in neurodegenerative diseases, inflammation, diabetes, and retinal diseases, other studies have described a deleterious role of αBC in cancers and pulmonary fibrosis. The therapeutic potential of αBC alone or in combination with αA-crystallin has been reported. Acetylated αBC peptides have been shown to be more potent than native αBC for chaperone as well as therapeutic activities using both in vitro and in vivo models. Further, for efficient delivery of α BC into cells, carrier molecules such as polylacticcoglycolic acid, polycaprolactone and cell penetration peptides have been used. In this review, we have summarized current data from emerging and exciting studies of the therapeutic strategies of α BC and α BC peptides and the efficient delivery strategies of these proteins in various disease models, including neurodegenerative diseases, retinal diseases, platelet aggregation, inflammation, and ischemia.
    No preview · Article · Jan 2015 · Current Molecular Medicine
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    ABSTRACT: Wip1 is a serine/threonine protein phosphatase which plays a critical role in neutrophil development and maturation. In the present study, we used a neutrophildependent model of intestinal ischemia/reperfusion (I/R) injury to identify the role of Wip1 in neutrophil function under the condition of oxidative stress and inflammation. Wip1- deficient mice displayed more severe intestinal I/R injury with increased infiltration of neutrophils and higher expression of chemokines like CXCL-1, CXCL-2 and CCL-2, as well as inflammatory cytokine like TNF-α and IL-17. Studies in Wip1KOa→WT full hematopoietic chimera mice showed that Wip1 intrinsically regulated the function of immune cells after intestinal I/R injury. Through adoptive transfer of neutrophils from WT mice or mice with deficiency of IL-17, IL-17/Wip1 or Wip1, we demonstrated that Wip1KO neutrophils produced more IL-17 and eventually led to more severe intestinal I/R injury. Thus, our findings identify Wip1 as an intrinsic negative regulator of neutrophil inflammation in intestinal I/R injury process.
    No preview · Article · Jan 2015 · Current Molecular Medicine

  • No preview · Article · Jan 2015 · Current Molecular Medicine