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Special Issue "Advanced Research on Chemokines and Chemokine Receptors"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 31 January 2024 | Viewed by 1284

Special Issue Editor

1. Musculoskeletal Disease Center, Research Service, VA Loma Linda Healthcare Systems, Loma Linda, CA 92357, USA
2. Department of Medicine, Loma Linda University, Loma Linda, CA 92354, USA
Interests: chemokines; chemokine receptors; inflammation; regeneration; inhibitors; stimulators; molecular signaling pathways

Special Issue Information

Dear Colleagues,

Chemokines belong to a family of small cytokines; they promote the directional migration of leukocytes, endothelial and epithelial cells through binding to their specific receptors. They share a typical key structure that is stabilized by disulfide bonds between the cysteine residues at the NH2-terminal of the protein. Chemokines are secreted by a great variety of cells. Their function is directly dependent on their interactions with their receptors. They are involved in many physiological processes, including but not limited to embryogenesis, bone remodeling, fracture healing and wound healing. They play a vital role in host defense mechanisms through the development and maintenance of innate and acquired immunity, but their chronic expression is linked with chronic diseases, delayed fracture and wound healing, and other health complications.

In this Special Issue entitled Advanced Research on Chemokines and Chemokine Receptors, we invite scientists to submit review articles and original research articles about the latest discoveries which further our understanding of the function and role of chemokines and their receptors in different physiological and pathological processes, and about studies which explore strategies for the development of new molecules or drugs to modulate chemokines’ functions.

Dr. Bouchra Edderkaoui
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • chemokines
  • chemokine receptors
  • chronic diseases
  • angiogenesis
  • fracture
  • regeneration
  • chemokine function
  • expression

Published Papers (1 paper)

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Fractalkine Improves the Expression of Endometrium Receptivity-Related Genes and Proteins at Desferrioxamine-Induced Iron Deficiency in HEC-1A Cells
Int. J. Mol. Sci. 2023, 24(9), 7924; https://doi.org/10.3390/ijms24097924 - 27 Apr 2023
Cited by 1 | Viewed by 991
Fractalkine (CX3CL1/FKN) is a unique chemokine belonging to the CX3C chemokine subclass. FKN exists in two forms: a membrane-bound form expressed by both endometrium cells and trophoblasts thought to be implicated in maternal–fetal interaction and a soluble form expressed by endometrium cells. Endometrium [...] Read more.
Fractalkine (CX3CL1/FKN) is a unique chemokine belonging to the CX3C chemokine subclass. FKN exists in two forms: a membrane-bound form expressed by both endometrium cells and trophoblasts thought to be implicated in maternal–fetal interaction and a soluble form expressed by endometrium cells. Endometrium receptivity is crucial in embryo implantation and a complex process regulated by large numbers of proteins, e.g., cytokines, progesterone receptor (PR), SOX-17, prostaglandin receptors (PTGER2), and tissue inhibitors of metalloproteinases (TIMPs). It has also been reported that iron is important in fertility and affects the iron status of the mother. Therefore, iron availability in the embryo contributes to fertilization and pregnancy. In this study, we focused on the effect of iron deficiency on the secreted cytokines (IL-6, IL-1β, leukocyte inhibitory factor, TGF-β), chemokines (IL-8, FKN), and other regulatory proteins (bone morphogenic protein 2, activin, follistatin, PR, SOX-17, prostaglandin E2 receptor, TIMP2), and the modifying effect of FKN on the expression of these proteins, which may improve endometrium receptivity. Endometrial iron deficiency was mediated by desferrioxamine (DFO) treatment of HEC-1A cells. FKN was added to the cells 24 h and 48 h after DFO with or without serum for modelling the possible iron dependence of the alterations. Our findings support the hypothesis that FKN ameliorates the effects of anemia on the receptivity-related genes and proteins in HEC-1A cells by increasing the secretion of the receptivity-related cytokines via the fractalkine receptor (CX3CR1). FKN may contribute to cell proliferation and differentiation by regulating activin, follistatin, and BMP2 expressions, and to implantation by altering the protein levels of PR, SOX-17, PTGER2, and TIMP2. FKN mitigates the negative effect of iron deficiency on the receptivity-related genes and proteins of HEC-1A endometrium cells, suggesting its important role in the regulation of endometrium receptivity. Full article
(This article belongs to the Special Issue Advanced Research on Chemokines and Chemokine Receptors)
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