Molecular Medicine Reports Journal Impact Factor & Information

Publisher: Spandidos Publications

Journal description

Current impact factor: 1.48

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 1.484
2012 Impact Factor 1.17
2011 Impact Factor 0.418
2010 Impact Factor 0.307
2009 Impact Factor 0.22
2008 Impact Factor 0

Impact factor over time

Impact factor

Additional details

5-year impact 0.96
Cited half-life 1.90
Immediacy index 0.26
Eigenfactor 0.00
Article influence 0.22
Website Molecular Medicine Reports website
ISSN 1791-2997
OCLC 248467032
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Spandidos Publications

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Publisher's version/PDF must be used
    • On Institutional Repository or Funder's repository
    • Must link to publisher version
    • Published source must be acknowledged with full citation
    • Publisher will automatically deposit authors post-print in PubMed Central or Europe PMC after 6 months or 12 months as required by funding agency
    • Reviewed 07 July 2014
  • Classification
    ​ white

Publications in this journal

  • Molecular Medicine Reports 08/2015; DOI:10.3892/mmr.2015.4242
  • Molecular Medicine Reports 08/2015; DOI:10.3892/mmr.2015.4218
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chondrosarcoma is one of the most common types of primary bone cancer that develops in cartilage cells. Resveratrol (Res), a natural polyphenol compound isolated from various fruits, has a suppressive effect on various human malignancies. It has been shown that Res inhibits matrix metalloproteinase (MMP)‑induced differentiation in chondrosarcoma cells. However, the effects of Res on cell proliferation, apoptosis and invasion of chondrosarcoma cells, as well as the underlying mechanisms, remain largely unknown. To the best of our knowledge, the present study showed for the first time that Res inhibited proliferation and induced apoptosis in chondrosarcoma cells in a dose-dependent manner. Furthermore, it was shown that Res also suppressed chondrosarcoma cell invasion in a dose-dependent manner, probably via the inhibition of MMP2 and MMP9 protein expression. Molecular mechanism investigations revealed that Res could inhibit the activity of phosphoinositide 3-kinase/AKT and p38 mitogen‑activated protein kinase signaling pathways, which has been demonstrated to be important in the regulation of proliferation, apoptosis and invasion in various cancer cell types. In conclusion, this study suggests that Res may serve as a promising agent for the treatment of chondrosarcoma.
    Molecular Medicine Reports 04/2015; 12(2). DOI:10.3892/mmr.2015.3683
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    ABSTRACT: Glucagon-like peptide-1 (GLP-1) analogues are likely to exert cardioprotective effects via balancing the energy metabolism in cardiomyocytes following ischemic or hypoxic insults. The present study aimed to explore the protective effects and mechanism of exendin‑4, a GLP‑1 analogue, on cardiomyocyte glucose uptake using an in vitro model of hypoxia/reoxygenation (H/R) of H9c2 cardiomyocyte cells. Pre‑treatment with exendin‑4 (200 nM) prior to H/R increased the cell viability, decreased cell apoptosis, enhanced cardiomyocyte glucose uptake and increased the production of adenosine triphosphate. Exendin‑4 also decreased the levels of lactate dehydrogenase and creatine kinase‑MB in the culture medium. Furthermore, the activity of carnitine palmitoyltransferase‑1 in the H9c2 cells was decreased, while the activity of phosphofructokinase‑1 was increased following exendin‑4 treatment. Moreover, pre‑treatment with exendin‑4 increased the expression of p38 mitogen‑activated protein kinase (p38MAPK) γ and translocation of glucose transporter‑1 in H9c2 cells subjected to H/R. However, these effects were attenuated by the p38MAPK inhibitors BIRB796 and SB203580. The results suggested that exendin‑4 exerted significant cardioprotective effects against H/R‑induced cell injury and restored the metabolic imbalance of cardiomyocytes by activating the p38MAPK signaling pathway in the H9c2 cell model. Importantly, p38MAPKγ, one subunit of p38MAPK, may have the most important function in this process. The results of the present study may be helpful in the development of novel drugs to treat patients with coronary heart disease.
    Molecular Medicine Reports 04/2015; DOI:10.3892/mmr.2015.3682
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    ABSTRACT: The aim of the present study was to enhance the efficiency of leukemia immunotherapy by increasing the antigen‑specific cytotoxic T lymphocyte‑inducing ability of leukemia cells. The leukemic plasmacytoid dendritic cell line PMDC05 containing the HLA‑A02/24 antigen, which was previously established in our laboratory (Laboratory of Hematology and Oncology, Graduate School of Health Sciences, Niigata University, Niigata, Japan), was used in the present study. It exhibited higher expression levels of CD80 following transduction with lentiviruses encoding the CD80 gene. This CD80‑expressing PMDC05 was named PMDC11. In order to establish a more potent antigen‑presenting cell for cellular immunotherapy of tumors or severe infections, PMDC11 cells were transduced with a constitutively active (ca) toll‑like receptor 4 (TLR4) gene using the Tet‑On system (caTLR4‑PMDC11). CD8+ T cells from healthy donors with HLA‑A02 were co‑cultured with mutant WT1 peptide‑pulsed PMDC11, lipopolysaccharide (LPS)‑stimulated PMDC11 or caTLR4‑PMDC11 cells. Interleukin (IL)‑2 (50 IU/ml) and IL‑7 (10 ng/ml) were added on day three of culture. Priming with mutant WT1 peptide‑pulsed PMDC11, LPS‑stimulated PMDC11 or caTLR4‑PMDC11 cells was conducted once per week and two thirds of the IL‑2/IL‑7 containing medium was replenished every 3‑4 days. Immediately prior to the priming with these various PMDC11 cells, the cultured cells were analyzed for the secretion of interferon (IFN)‑γ in addition to the percentage and number of CD8+/WT1 tetramer+ T cells using flow cytometry. caTLR4‑PMDC11 cells were observed to possess greater antigen‑presenting abilities compared with those of PMDC11 or LPS‑stimulated PMDC11 cells in a mixed leukocyte culture. CD8 T cells positive for the WT1 tetramer were generated following 3‑4 weeks of culture and CD8+/WT1 tetramer+ T cells were markedly increased in caTLR4‑PMDC11‑primed CD8+ T cell culture compared with PMDC11 or LPS‑stimulated PMDC11‑primed CD8+ T cell culture. These CD8+ T cells co‑cultured with caTLR4‑PMDC11 cells were demonstrated to secrete IFN‑γ and to be cytotoxic to WT1‑expressing target cells. These data suggested that the antigen‑specific cytotoxic T lymphocyte (CTL)‑inducing ability of PMDC11 was potentiated via transduction of the caTLR4 gene. The present study also suggested that caTLR4‑PMDC11 cells may be applied as potent antigen‑presenting cells for generating antigen‑specific CTLs in adoptive cellular immunotherapy against tumors and severe viral infections.
    Molecular Medicine Reports 04/2015; DOI:10.3892/mmr.2015.3685
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    ABSTRACT: Latent infection with adenovirus and respiratory syncytial virus (RSV) is associated with chronic obstructive pulmonary disease (COPD). The role of respiratory viral infections are emerging in COPD exacerbations. The present study aimed to investigate the prevalence of adenovirus and RSV serotypes A and B in individuals with acute exacerbations of COPD (COPD‑AE) and stable COPD. Twenty seven patients with COPD‑AE were evaluated using a prospective longitudinal study design. Induced sputum, sera and nasal smears were sampled from patients experiencing COPD‑AE and those in a stable condition. Adenoplex® multiplex polymerase chain reaction (PCR) kits and Invitek RTP® DNA/RNA Virus Mini kits were used for PCR assays of adenovirus and RSV, respectively. Eighteen patients who experienced a COPD‑AE were also evaluated while in a stable condition. The results showed that three sputum samples were positive for adenovirus in patients experiencing an exacerbation, while one was positive among the patients in a stable condition. RSV serotype A was detected in 17/27 (63%) patients with COPD‑AE and 10/18 (55.6%) patients in a stable condition. RSV serotype B was not detected. Patients with COPD‑AE, who were positive for RSV serotype A exhibited higher serum fibrinogen levels than those who were negative (438.60±126.08 mg/dl compared with 287.60±85.91 mg/dl; P=0.004). Eight/ten patients who were positive for RSV serotype A while in a stable condition, were also positive during COPD‑AE. The results of the present study suggested that RSV infection may be prevalent in patients with COPD‑AE and in those in a stable condition. Therefore, chronic RSV infection may occur in COPD. The detection and prevention of RSV may be useful in the management of COPD.
    Molecular Medicine Reports 04/2015; DOI:10.3892/mmr.2015.3681
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    ABSTRACT: The present study aimed to determine whether artesunate has beneficial effects on bleomycin‑induced pulmonary fibrosis in rats and to examine the possible mechanisms underlying these effects. All experiments were performed with male Sprague Dawley rats weighing 180‑250 g. Animals were randomly divided into four experimental groups that were administered either saline alone, artesunate alone, bleomycin alone or bleomycin + artesunate. Lung histopathology was investigated by hematoxylin and eosin staining and Masson staining. Lung profibrotic molecules were analyzed by reverse transcription polymerase chain reaction, immunoblotting and immunohistochemistry. In rats treated with artesunate, pulmonary fibrosis induced by bleomycin was significantly reduced. Administration of artesunate significantly improved bleomycin‑induced morphological alterations. Profibrotic molecules, including transforming growth factor‑β1, Smad3, heat shock protein 47, α‑smooth muscle actin and collagen type I were also reduced by artesunate. These findings suggest that artesunate improves bleomycin‑induced pulmonary fibrosis pathology in rats possibly by inhibiting profibrotic molecules associated with pulmonary fibrosis.
    Molecular Medicine Reports 03/2015; DOI:10.3892/mmr.2015.3500
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    ABSTRACT: The aim of the present study was to investigate the association of neonatal necrotizing enterocolitis (NEC) with myeloid differentiation‑(MD‑2) and GM2 activator protein (GM2A) genetic polymorphisms. Gene resequencing of the MD‑2 and GM2A gene exons was performed on 42 neonates, diagnosed with NEC (NEC group), as well as in the rs11465996 locus, located in the MD‑2 gene promoter region. The aim was to detect the genetic polymorphisms present in the neonates with NEC and compare the functional polymorphic loci with 83 neonates without NEC (control group), who had been born during the same period. A polymorphic locus with abnormal frequency was detected in the exon region of the MD‑2 gene. In the NEC group, the frequency of genotypes carrying the low frequency allele (G) in the rs11465996 locus (MD‑2 promoter region) was significantly higher compared with the control group (χ2=4.388, P=0.036). Furthermore, the frequencies of genotypes carrying the low frequency A and C alleles in the rs1048719 (GM2A gene exon 1) and rs2075783 loci (GM2A intron), respectively, were significantly higher in the NEC group compared with the control group (χ2=4.316, P=0.038; and χ2=13.717, P=0.000, respectively). In addition, the rs11465996 polymorphism in the MD‑2 gene promoter region was found to be associated with the severity of NEC. Furthermore, the rs2075783 polymorphism in the GM2A gene exon 1 and the rs1048719 polymorphism in the intron region of this gene, were associated with the occurrence of NEC. The present study demonstrated that gene polymorphisms of MD‑2 and GM2A were associated with the occurrence or severity of NEC; however, further in‑depth exploration is required to clarify the associations between genetic predispositions to polymorphisms, and NEC.
    Molecular Medicine Reports 03/2015; DOI:10.3892/mmr.2015.3499
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    Molecular Medicine Reports 02/2015; DOI:10.3892/mmr.2015.3355
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    Molecular Medicine Reports 02/2015; DOI:10.3892/mmr.2015.3346
  • Molecular Medicine Reports 01/2015; DOI:10.3892/mmr.2015.3205
  • Molecular Medicine Reports 01/2015; in press.
  • Chueh · Lin · Weng · Huang · Chung
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    ABSTRACT: Polygonum cuspidatum is a natural plant that is used in traditional Chinese herbal medicine. The crude extract of Polygonum cuspidatum (CEPC) has numerous biological effects; however, there is a lack of studies on the effects of CEPC on immune responses in normal mice. The aim of the present study was to determine the in vivo effects of CEPC on immune responses in normal mice. CEPC (0, 50, 100, 150 and 200 mg/kg) was orally administered to BALB/c mice for three weeks, following which blood, liver, and spleen samples were collected. CEPC did not significantly affect the total body weight, or tissue weights of the liver or spleen, as compared with the control mice. CEPC increased the percentages of CD3 (Tcell marker), 11b (monocytes) and Mac3 (macrophages) positivecells, and reduced the percentage of CD19positive cells (Bcell marker), as compared with the control mice. CEPC (100 mg/kg) stimulated macrophage phagocytosis of blood samples but did not affect macrophage phagocytosis in the peritoneum. Activity of the splenic natural killer cells was increased in response to CEPC (50 mg/kg) treatment. Furthermore, CEPC inhibited T and Bcell proliferation when the cells were stimulated with concanavalin A and lipopolysaccharide, respectively.
    Molecular Medicine Reports 01/2015; 11(1). DOI:10.3892/mmr.2014.2739
  • Cheng · Wan · Xu · Zhou · Wang · Zhu
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    ABSTRACT: Melatonin (MLT) is an endogenous indole compound with numerous biological activities that has been associated with atherosclerosis (AS). In the present study, rabbits were used as an AS model in order to investigate whether MLT affects endothelial cell permeability, myosin light chain kinase (MLCK) activity and MLCK expression via the mitogenactivated protein kinase (MAPK) pathway. Expression and activity of MLCK were measured using western blot analysis, quantitative polymerase chain reaction, immunohistochemistry and γ32Padenosine triphosphate incorporation. Endothelial permeability was detected using rhodamine phalloidin fluorescence staining. The phosphorylation of extracellular regulated protein kinase (ERK), cJun Nterminal kinase (JNK) and p38 in endothelial cells were also analyzed using western blot analysis. Atheromatous plaques were formed in rabbits with a high cholesterol diet; however, following treatment with MLT, the number and areas of atheromatous plaques were significantly reduced. In addition, MLT treatment reversed the increase of MLCK activity and expression that occurred in rabbits with high cholesterol intake. Furthermore, levels of phosphorylated ERK, JNK and p38 decreased following MLT treatment. In conclusion, the results of the present study indicated that AS may be associated with increased MLCK expression and activity, which was reduced following treatment with MLT. The mechanism of action of MLT was thought to proceed via modulating MAPK pathway signal transduction; however, further studies are required in order to fully elucidate the exact regulatory mechanisms involved.
    Molecular Medicine Reports 01/2015; 11(1). DOI:10.3892/mmr.2014.2753
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    ABSTRACT: This study aimed to investigate the effects of BMSCs that had been pretreated with pioglitazone and/or rosiglitazone on the growth and proliferation rate of MCF-7 cells. The adhesive stem-and-cancer cell interaction showed that the pretreatment of BMSCs with a combination of two TZDs reduced the growth of MCF-7 cells. However, the proliferation rate of MCF-7 cells could be reduced by the non-adhesive interaction of the cancer cells with BMSCs pretreated with pioglitazone and/or rosiglitazone. The growth reduction effects on the growth and proliferation rate may be attributed to the reduction of the FGF4 protein level in the conditioned medium of the pretreated BMSCs. The fact that the low FGF4 protein level in the conditioned medium of the pretreated BMSCs perturbed the proliferation rate of MCF-7 cells by reducing the levels of Ki-67 and PCNA transcripts in the cancer cells was also shown in this study using a FGF4 neutralizing antibody. All of the above findings demonstrate that future studies on the correlation between FGF4 and pretreated BMSCs would be beneficial.
    Molecular Medicine Reports 01/2015;