International Journal of Molecular Medicine Impact Factor & Information

Publisher: Panepistēmio tēs Krētēs, Spandidos Publications

Journal description

Current impact factor: 2.09

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.088
2013 Impact Factor 1.88
2012 Impact Factor 1.957
2011 Impact Factor 1.573
2010 Impact Factor 1.814
2009 Impact Factor 1.98
2008 Impact Factor 1.88
2007 Impact Factor 1.847
2006 Impact Factor 1.854
2005 Impact Factor 2.09
2004 Impact Factor 3.19
2003 Impact Factor 1.94
2002 Impact Factor 2.063
2001 Impact Factor 1.689
2000 Impact Factor 1.899
1999 Impact Factor 1.058
1998 Impact Factor

Impact factor over time

Impact factor

Additional details

5-year impact 2.01
Cited half-life 5.60
Immediacy index 0.44
Eigenfactor 0.01
Article influence 0.48
Website International Journal of Molecular Medicine website
Other titles International journal of molecular medicine (Online)
ISSN 1107-3756
OCLC 53915595
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

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

  • International Journal of Molecular Medicine 09/2015; DOI:10.3892/ijmm.2015.2359
  • International Journal of Molecular Medicine 09/2015; DOI:10.3892/ijmm.2015.2356
  • International Journal of Molecular Medicine 09/2015; DOI:10.3892/ijmm.2015.2354
  • [Show abstract] [Hide abstract]
    ABSTRACT: Spinal cord injury (SCI) leads to the loss of structure and function of axons. However, injured axons cannot grow or regenerate spontaneously following injury. Generally, only when treated with neurotrophins, such as nerve growth factor (NGF), will the neurons sprout new axons. Akt is one of the central kinases of neurocytes. PC12 cells are a frequently used cell model for neural differentiation and development studies. The nuclear factor erythroid 2‑related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway is a main mechanism in prevention from oxidative stress, which may damage the nervous system. The present study employed this cell model to investigate whether Akt could induce axon growth in PC12 cells on the basis of NGF treatments. The results showed that Akt overexpression significantly increased cell proliferation and decreased cell apoptosis. Additionally, Akt overexpression activated Nrf2/ARE pathways. In conclusion, the experiments indicated that Akt overexpression contributed to axon regeneration induced by NGF in PC12 cells through activating the Nrf2/ARE pathway.
    International Journal of Molecular Medicine 08/2015; DOI:10.3892/ijmm.2015.2329
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    ABSTRACT: Dental pulp cells (DPCs), including dental pulp (DP) stem cells, play a role in dentine repair under certain conditions caused by bacterial infections associated with caries, tooth fracture and injury. Mesenchymal stem cells (MSCs) have also been shown to be involved in this process of repair. However, the mechanisms through which MSCs are recruited to the DP have not yet been elucidated. Therefore, the aim of the present in vitro study was to investigate whether stromal cell‑derived factor 1α (SDF1)-C-X-C chemokine receptor type 4 (CXCR4) signaling is involved in tissue repair in the DP of deciduous teeth. A single-cell clone from DPCs (SDP11) and UE7T-13 cells were used as pulp cells and MSCs, respectively. The MG-63 and HuO9 cells, two osteosarcoma cell lines, were used as positive control cells. Reverse transcription polymerase chain reaction (RT‑PCR) revealed that all cell lines (SDP11, UE7T-13 MG-63 and HuO9) were positive for both SDF1 and CXCR4 mRNA expression. Moreover, immunocytochemical analysis indicated that SDF1 and CXCR4 proteins were expressed in the SDP11 and UE7T-13 cells. SDF1 was also detected in the cell lysates (CLs) and conditioned medium (CM) collected from the SDP11 and UE7T-13 cells, and AMD3100, a specific antagonist of CXCR4, inhibited the migration of the UE7T-13 cells; this migration was induced by treatment with CM, which was collected from the SDP11 cells. In addition, real-time PCR showed that the expression of SDF1 in the SDP11 cells was inhibited by treatment with 20 ng/ml fibroblast growth factor (FGF)-2, and exposure to AZD4547, an inhibitor of the FGF receptor, blocked this inhibition. Collectively, these data suggest that SDF1 produced by DP plays an important role in homeostasis, repair and regeneration via the recruitment of MSCs.
    International Journal of Molecular Medicine 06/2015; in press(2). DOI:10.3892/ijmm.2015.2247
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    ABSTRACT: Aldosterone is a steroid hormone secreted from the adrenal cortex, which regulates blood pressure. Higher concentrations of aldosterone can cause several diseases, including hypertension, diabetic nephropathy and chronic kidney disease. Previous reports have demonstrated that aldosterone has a pathogenic role in renal injury via reactive oxygen species (ROS), which involves the regulation of autophagy. However, whether aldosterone can induce autophagy in renal tubular cells remains to be elucidated. In the present study, elevated autophagy was observed in rat renal tubular NRK-52E cells exposed to aldosterone, which was demonstrated by the increased number of autophagosomes, conversion of LC3-I to LC3-II and the expression of Beclin-1. The enhanced autophagy was accompanied by increased production of intracellular ROS, which was reversed by N-acetylcysteine, a specific inhibitor of ROS signaling. Furthermore, treatment with ginsenoside Rg1 reduced the aldosterone-induced autophagy and production of ROS, possibly through reducing the phosphorylation of AMPK and preserving mTOR activity. These findings demonstrated that aldosterone promoted ROS generation and increased autophagy in the NRK-52E cells. Ginsenoside Rg1 effectively relieved aldosterone-induced oxidative stress and abnormal autophagy, suggesting that Rg1 may be used as a potential therapeutic drug to inhibit the renal injury, which is induced by aldosterone.
    International Journal of Molecular Medicine 06/2015; 36(2). DOI:10.3892/ijmm.2015.2242
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    ABSTRACT: Persistent investigations for the identification of novel anti-herpetic drugs are being conducted worldwide, as current treatment options are sometimes insufficient. The immunomodulator, ammonium trichloro[1,2‑ethanediolato‑O,O']‑tellurate (AS101), a non‑toxic tellurium (Ⅳ) compound, has been shown to exhibit anti‑viral activity against a variety of viruses in cell cultures and in animal models. In the present study, the anti‑viral activity of AS101 against herpes simplex virus (HSV)‑1 and 2 was investigated in vitro. The results demonstrated that AS101 significantly restricted HSV‑2-induced plaque formation and reduced the infectivity of the HSV‑2 yield, while HSV‑1 was affected to a lesser extent. The incubation of mature HSV‑1 and HSV‑2 viruses with AS101 had no effect on viral infectivity, indicating that the compound interrupts de novo viral synthesis. The addition of AS101 at up to 9 h post‑infection had almost the same effect as did the addition of the drug together with the virus (it maintained 80% of its total anti‑viral capacity). Quantitative PCR and immunofluoresence staining of viral structural proteins revealed that the viral DNA and protein synthesis stages were not interrupted by the administration of AS101. By contrast, in the presence of the compound, significantly fewer viable viruses (≥2 log reduction) were recovered from the AS10‑treated cell cultures. Of note, when we determined the viability of the intracellular virus, formed in the presence of the compound, a less severe (≤1 log) effect was observed. Taken together, these data strongly suggest that AS101 primarily interferes with late stages of viral replication, such as viral particle envelopment or egress, leading to the production of a defective virus progeny.
    International Journal of Molecular Medicine 04/2015; 36(1). DOI:10.3892/ijmm.2015.2197
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    ABSTRACT: Obstructive sleep apnea, characterized by recurrent episodes of hypoxia [intermittent hypoxia (IH)], has been identified as a risk factor for cardiovascular diseases. The O-linked β-N-acetylglucosamine (O-GlcNAc) modification (O-GlcNAcylation) of proteins has important regulatory implications on the pathophysiology of cardiovascular disorders. In this study, we examined the role of O-GlcNAcylation in cardiac architecture and left ventricular function following IH. Rats were randomly assigned to a normoxia and IH group (2 min 21% O2; 2 min 6-8% O2). Left ventricular function, myocardial morphology and the levels of signaling molecules were then measured. IH induced a significant increase in blood pressure, associated with a gradually abnormal myocardial architecture. The rats exposed to 2 or 3 weeks of IH presented with augmented left ventricular systolic and diastolic function, which declined at week 4. Consistently, the O-GlcNAc protein and O-GlcNAcase (OGA) levels in the left ventricular tissues steadily increased following IH, reaching peak levels at week 3. The O-GlcNAc transferase (OGT), extracellular signal-regulated kinase 1/2 (ERK1/2) and the p38 mitogen-activated protein kinase (p38 MAPK) phosphorylation levels were affected in an opposite manner. The phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII) remained unaltered. In parallel, compared with exposure to normoxia, 4 weeks of IH augmented the O-GlcNAc protein, OGT, phosphorylated ERK1/2 and p38 MAPK levels, accompanied by a decrease in OGA levels and an increase in the levels of myocardial nuclear factor-κB (NF-κB), inflammatory cytokines, caspase-3 and cardiomyocyte apoptosis. Taken together, our suggest a possible involvement of O-GlcNAc protein and MAPK signaling in the alterations of left ventricular function and cardiac injury following IH.
    International Journal of Molecular Medicine 04/2015; 36(1). DOI:10.3892/ijmm.2015.2198
  • International Journal of Molecular Medicine 04/2015; in press.
  • International Journal of Molecular Medicine 04/2015; in press.
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    ABSTRACT: Semaphorin 3A (SEMA3A) was initially identified to play an important role in axonal guidance. Recently, SEMA3A has also been considered as a candidate tumor suppressor, since it is often downregulated in numerous types of cancer, including prostate cancer, breast cancer and glioma. However, the biological role of SEMA3A in ovarian cancer is not clear. In the present study, the expression of SEMA3A in ovarian cancer and normal ovarian epithelial tissues was detected by immunofluorescence, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting, and the associations between the expression of SEMA3A with the development of ovarian cancer, clinicopathological characteristics and survival were also analyzed. Results from immunofluorescence, RT‑qPCR and western blotting showed that SEMA3A is significantly downregulated in epithelial ovarian carcinoma compared to normal ovarian epithelial specimens (P<0.05). The expression levels of SEMA3A were lower in the cancer tissues with III/IV stage [the International Federation of Gynecology and Obstetrics (FIGO) stage], poor histological grade, lymph node metastasis and distant metastasis compared to that in the cancer tissues with I/II stage (FIGO), well histological grade, or without lymph node metastasis and distant metastasis (P<0.05). A decreased expression of SEMA3A is associated with a poor prognosis (P<0.001). The present findings suggest that decreased SEMA3A expression may be associated with the development of epithelial ovarian carcinoma, and therefore, SEMA3A may be a valuable prognostic marker, as well as a potential molecular therapy target for ovarian cancer patients.
    International Journal of Molecular Medicine 03/2015; 35(5). DOI:10.3892/ijmm.2015.2142
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    ABSTRACT: Angiotensin II (AngII) is the central product of the renin‑angiotensin system (RAS) and this octapeptide contributes to the pathophysiology of cardiac hypertrophy and remodeling. mAKAPβ is an A‑kinase anchoring protein (AKAP) that has the function of binding to the regulatory subunit of protein kinase A (PKA) and confining the holoenzyme to discrete locations within the cell. In this study, we aimed to investigate the role of mAKAPβ in AngII‑induced cardiomyocyte hypertrophy and the possible mechanisms involved. Cultured cardiomyocytes from neonatal rats were treated with AngII. Subsequently, the morphology of the cardiomyocytes was observed and the expression of mAKAPβ and cardiomyocyte hypertrophic markers was measured. mAKAPβ‑shRNA was constructed for RNA interference; the expression of mAKAPβ and hypertrophic markers, the cell surface area and the [3H]Leucine incorporation rate in the AngII‑treated rat cardiomyocytes were detected following RNA interference. Simultaneously, changes in the expression levels of phosphorylated extracellular signal-regulated kinase (p‑ERK)2 in the cardiomyocytes were assessed. The cell size of the AngII-treated cardiaomyocytes was significantly larger than that of the untreated cardiomyocytes. The expression of hypertrophic markers and p‑ERK2, the cell surface area and the [3H]Leucine incorporation rate were all significantly increased in the AngII‑treated cells. However, the expression of mAKAPβ remained unaltered in this process. RNA interference simultaneously inhibited the protein expression of mAKAPβ and p‑ERK2, and the hypertrophy of the cardiomyocytes induced by AngII was attenuated. These results demonstrate that AngII induces hypertrophy in cardiomyocytes, and mAKAPβ is possibly involved in this process. The effects of mAKAPβ on AngII‑induced cardiomyocyte hypertrophy may be associated with p‑ERK2 expression.
    International Journal of Molecular Medicine 03/2015; 35(5). DOI:10.3892/ijmm.2015.2119
  • International Journal of Molecular Medicine 01/2015; In press..
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    ABSTRACT: Taurine (Tau), the most abundant free amino acid in humans has numerous potential health benefits through its antioxidant and anti‑inflammatory properties. However, limited studies have assessed its effect on tumors and the antitumor mechanism remains unknown. The present study investigated the cellular and molecular changes induced by Tau, leading to the induction of apoptosis in human breast cancer cell lines MCF‑7 and MDA‑MB‑231. MCF‑7 is p53 proficient (p53+/+) and MDA‑MB‑231 is a p53 null mutant (p53-/-). Cell proliferation and viability were assessed by MTT. Flow cytometry and hoechst33342 fluorescent staining were employed to detect apoptosis. Spectrophotometry was used to detect caspase‑3 activity. Reverse transcription‑polymerase chain reaction and western blot analysis were used to detect the levels of mRNA and proteins of p53‑upregulated modulator of apoptosis (PUMA), Bax and Bcl‑2. Finally, the affect of Tau on the growth of MDA‑MB‑231‑cell‑nude mice xenografts was examined. In the study, Tau inhibited growth and induced apoptosis of the two cell lines in a concentration‑ and time‑dependent manner. Notably, the inhibitory effect of Tau on p53-/- cancer cells was clearly significant compared to the p53+/+ cancer cells. Further studies showed that Tau promoted apoptosis in human breast cancer cells and inhibited the growth of tumor in nude mice by inducing the expression of PUMA, which further up‑ and downregulated the expression of Bax and Bcl‑2 protein, giving rise to increased activation of caspase‑3. Collectively, these results indicate that Tau is a potent candidate for the chemotherapy of breast cancer through increasing the PUMA expression independent of p53 status.
    International Journal of Molecular Medicine 11/2014; 35(1). DOI:10.3892/ijmm.2014.2002
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    ABSTRACT: The use of peptide‑based vaccines as therapeutics aims to elicit immune responses through antigenic epitopes derived from tumor antigens. Peptide‑based vaccines are easily synthesized and chemically stable entities, and of note, they are absent of oncogenic potential. However, their application is more complicated as the success of an effective peptide‑based vaccine is determined by numerous parameters. The success thus far has been limited by the choice of tumor antigenic peptides, poor immunogenicity and incorporation of strategies to reverse cancer‑mediated immune suppression. In the present review, an overview of the mechanisms of peptide‑based vaccines is provided and antigenic peptides are categorized with respect to their tissue distribution in order to determine their usefulness as targets. Furthermore, certain approaches are proposed that induce and maintain T cells for immunotherapy. The recent progress indicates that peptide‑based vaccines are preferential for targeted therapy in cancer patients.
    International Journal of Molecular Medicine 11/2014; 35(1). DOI:10.3892/ijmm.2014.2000