Aims & Scope:

Current Molecular Medicine is an interdisciplinary journal focused on providing the readership with current and comprehensive reviews, original research articles, short communications/letters and drug clinical trial studies 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 invites guest editors to devote an issue 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.




MOST ACCESSED ARTICLE – Blood Flow Regulates Zebrafish Caudal Vein Plexus Angiogenesis by ERK5-klf2a-nos2b Signaling

Journal Name: Current Molecular Medicine

Author(s): X. Xie, T. Zhou, Y. Wang, H. Chen, D. Lei, L. Huang, Y. Wang, X. Jin, T. Sun, J. Tan, T. Yin, J. Huang, H. Gregersen, G. Wang*.




Background: Vascular network formation induced by angiogenesis plays an important role in many physiological and pathological processes. However, the role of blood flow and underlying mechanisms in vascular network formation, for example for the development of the caudal vein plexus (CVP), is poorly understood.

Objective: The aim of this study was to explore the role of ERK5-klf2a-nos2b signaling in the CVP angiogenesis.

Method and Results: In this study on tnnt2a-MO injection and chemical blood flow modulator treatment in zebrafish embryos, we demonstrated that decreased blood flow disrupted CVP formation. The hemodynamic force was quantitatively analyzed. Furthermore, CVP angiogenesis in zebrafish embryos was inhibited by disruption of the blood flow downstream effectors ERK5, klf2a, and nos2b in response to treatment with the ERK5 specific inhibitor and to injection of klf2a-MO, nos2b-MO. Overexpression of klf2a mRNA or nos2b mRNA restored vascular defects in tnnt2a or klf2a morphants. The data suggest that flow-induced ERK5-klf2a-nos2b signaling is involved in CVP angiogenesis in zebrafish embryos.

Conclusion: We have demonstrated that blood flow is essential for vascular network formation, specifically for CVP angiogenesis in zebrafish. A novel genetic and mechanical mechanism was discovered in which ERK5 facilitates the integration of blood flow with the downstream klf2a-nos2b signaling for CVP angiogenesis.



OPEN ACCESS ARTICLE – Decreased Expression of TIM-3 on Th17 Cells Associated with Ophthalmopathy in Patients with Graves’ Disease

Journal Name: Current Molecular Medicine

Author(s): J. Zhao, B. Lin, H. Deng, X. Zhi, Y. Li, Y. Liu, P.W. Bible, Q. Li, B. Xu, L. Wei, H. Yang*, D. Huang*.





Purpose: Thyroid-associated Ophthalmopathy (TAO) is one of the most common orbital immunological diseases in adults. CD4+ helper T (Th) cells play important roles in the pathogenesis of TAO. But the mechanisms regulating CD4+ T cell activity is unclear. This study examines T cell immunoglobulin domain and mucin domain 3 (TIM-3) expression in helper T cell type 1 (Th1), Th17, and regulatory T cells in sufferers of TAO.

Methods: Participants were divided into 3 groups: patients with TAO, patients with Graves’ disease but without orbitopathy (GD), and healthy control patients (HC). Peripheral blood samples were collected for each patient in the designated group. Flow cytometry methods assessed the frequency of Th1 (CD4+IFN-γ+), Th17 (CD4+IL-17+), regulatory T cells (CD4+CD25hiCD127lo), and TIM-3 protein expression. Mean fluorescence intensity (MFI) measured the magnitude of TIM-3 expression and the percentage of TIM-3+ cells for each patient.

Results: Compared to the GD group, TAO patients possessed higher frequencies of Th1 and Th17 cells in peripheral blood samples. The percentage of TIM-3+ Th1 and Th17 cells was significantly lower in the TAO patients than the GD group. Across all patients sampled, TIM-3+ cell percentage negatively correlated with Th1 cell frequency. Th1 and Th17 cells exhibited significantly decreased expression of TIM-3 in TAO patients compared to healthy controls. Regulatory T cells showed little TIM-3 expression and we observed no significant differences in frequency between groups.

Conclusion: These results suggest a role for TIM-3 in the regulation of Th1 and Th17 cells and the pathogenesis of Graves’ ophthalmopathy.

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Current Molecular Medicine 17, Issue 8

Current Medicinal Chemistry 25, Issue 7

Anti-Cancer Agents in Medicinal Chemistry 18, Issue 1

Mini-Reviews in Medicinal Chemistry 18, Issue 6

Current Medicinal Chemistry 25, Issue 8

Current Drug Targets 19, Issue 5 



EDITOR’S CHOICE – Role of Zebrafish fhl1A in Satellite Cell and Skeletal Muscle Development – Current Molecular Medicine

Journal: Current Molecular Medicine

Author(s):  F. Chen, W. Yuan, X. Mo, J. Zhuang, Y. Wang, J. Chen, Z. Jiang, X. Zhu, Q. Zeng, Y. Wan, F. Li, Y. Shi, L. Cao, X. Fan, S. Luo, X. Ye, Y. Chen, G. Dai, J. Gao, X. Wang, H. Xie*, P. Zhu*, Y. Li*, X. Wu


Background: Four-and-a-half LIM domains protein 1 (FHL1) mutations are associated with human myopathies. However, the function of this protein in skeletal development remains unclear.

Methods: Whole-mount in situ hybridization and embryo immunostaining were performed.

Results: Zebrafish Fhl1A is the homologue of human FHL1. We showed that fhl1A knockdown causes defective skeletal muscle development, while injection with fhl1A mRNA largely recovered the muscle development in these fhl1A morphants. We also demonstrated that fhl1A knockdown decreases the number of satellite cells. This decrease in satellite cells and the emergence of skeletal muscle abnormalities were associated with alterations in the gene expression of myoD, pax7, mef2ca and skMLCK. We also demonstrated that fhl1A expression and retinoic acid (RA) signalling caused similar skeletal muscle development phenotypes. Moreover, when treated with exogenous RA, endogenous fhl1A expression in skeletal muscles was robust. When treated with DEAB, an RA signalling inhibitor which inhibits the activity of retinaldehyde dehydrogenase, fhl1A was downregulated.

Conclusion: fhl1A functions as an activator in regulating the number of satellite cells and in skeletal muscle development. The role of fhl1A in skeletal myogenesis is regulated by RA signaling.

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Recent Patents on Engineering 12-1

Current Molecular Medicine 17-7

Letters in Organic Chemistry 15-4

Letters in Drug Design & Discovery 15-4

Current Pharmaceutical Biotechnology 18-12


EDITOR’S CHOICE – Neuronal Expression of Junctional Adhesion Molecule-C is Essential for Retinal Thickness and Photoreceptor Survival – Current Molecular Medicine

Journal: Current Molecular Medicine

Author(s): Y. Li, F. Zhang, W. Lu*, X. Li*


Background: Photoreceptor cell death is a key pathology of retinal degeneration diseases. To date, the molecular mechanisms for this pathological process remain largely unclear. Junctional adhesion molecule-c (Jam-c) has been shown to play important roles in different biological events. However, its effect on retinal neuronal cells is unknown.

Objective: To determine the effect of Jam-c on adult mouse eyes, particularly, on retinal structure, vasculature and photoreceptor cells, in order to explore potential important target molecules for ocular diseases.

Methods: Jam-c global knockout mice, endothelial-specific and neuronal-specific Jam-c conditional knockout mice using Tie2-Cre and Nestin-Cre mice respectively were used in this study. Mouse eyes were harvested from the different groups and eye size examined. Cryosections of the eyes were made and stained with Hematoxylin and Eosin (H&E) and the thicknesses of retinal layers measured. Retinal blood vessels and cone and rod photoreceptors were analyzed using isolectin B4, peanut agglutinin and rhodopsin as markers respectively. In vivo Jam-c knockdown in mouse eyes was performed by intravitreal injection of Jam-c shRNA. Jam-c expression in the retinae was quantified by real-time PCR.

Results: Global Jam-c gene deletion in mice resulted in smaller eyes and decreased the diameters of lens and iris. Jam-c-/- mice display marked thinning of the outer nuclear layer (ONL), less numbers of photoreceptor cells, and abnormal retinal vasculature. Importantly, neuronal-specific Jam-c deletion led to similar phenotype, whereas no obvious defect was observed in endothelial-specific Jam-c knockout mice. Moreover, Jam-c knockdown by shRNA also decreased ONL thickness and photoreceptor numbers.

Conclusion: We found that Jam-c is critically required for the normal size and retinal structure. Particularly, Jam-c plays important roles in maintaining the normal retinal thickness, vasculature and photoreceptor numbers. Jam-c thus may therefore have important roles in various ocular diseases.

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World Glaucoma Week 2018!


World Glaucoma Week is observed from 8th March to 15th March, 2018. Glaucoma, is an eye diseases that is associated with elevated intraocular pressure, in which damage to the eye (optic) nerve can lead to loss of vision. Glaucoma is the leading cause of irreversible blindness in the world.

Bentham Science publishes papers from prominent medical researchers on Glaucoma. For the best published articles view the following journals:

Current Molecular Medicine 

Infectious Disorders – Drug Targets


Medicinal Chemistry Volume 14, Issue 2

Clinical Immunology, Endocrine & Metabolic Drugs Volume 4, Issue 1

Anti-Cancer Agents in Medicinal Chemistry Volume 17, Issue 14

Letters in Organic Chemistry Volume 15, Issue 3

Current Molecular Medicine Volume 17, Issue 6

Protein & Peptide Letters Volume 24, Issue 12



Current Physical Chemistry 7 – 4

MicroRNA 6 – 3

Current Molecular Medicine 17 – 4

Mini-Reviews in Medicinal Chemistry 18 – 1

Current Cancer Drug Targets 18 – 1

Letters in Organic Chemistry  15 – 1

Current Pharmaceutical Analysis 14 – 1

Current Green Chemistry 4 – 2

Endocrine, Metabolic & Immune Disorders – Drug Targets 18 – 1

Cardiovascular & Hematological Disorders-Drug Targets 17-2