Special Issue "Signal Transduction of Tissue Repair"
Deadline for manuscript submissions: closed (30 July 2014)
Dr. Regina M. Day
Department of Pharmacology, The Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814, USA
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Interests: cell biology and signal transduction of normal tissue repair and fibrotic remodeling in the lung; adult stem cells that participate in lung repair; apoptosis; cytoskeletal rearrangement; cellular senescence and inflammation; reactive oxygen species in signal transduction and antioxidant cellular defenses
Tissue homeostasis requires the capacity for normal repair. In a number of tissues, repair processes have been demonstrated to involve complex and sometimes interrelated events, including signaling from the initial injury, inflammation, cell recruitment and proliferation, and eventually remodeling or restoration of normal tissue. Although initial stages of tissue repair also involve inflammatory responses and the activation of mesenchymal cells, specific inhibitory signals are required to ensure that overwhelming levels of inflammation and fibrotic repair to not predominate, which would result in scarring and dysfunctional tissue. Different tissues in the adult vary greatly in their ability to regenerate normal architecture with normal function. For instance, the liver displays robust repair functions, while tissues such as the heart and lungs have more limited repair capabilities. Research investigating tissue regeneration has revealed a number of factors affect repair activities, including the abundance or paucity of specific adult stem cells, vascularization, microenvironment alterations, and the production of growth factors to effectively induce proliferation of the appropriate cell types for repair. This Special Issue will examine signal transduction pathways involved in tissue repair. In this issue, an emphasis will be placed on research and review articles examining mechanisms of signal transduction involved in normal tissue repair pathways, including those shown to induce proliferation and migration of adult stem cells. Signaling networks that govern wound and repair microenvironments, mesencymal-epithelial transition (MET) for the generation of pluripotent stem cells, and the regulation of factors and cytokines required for tissue repair will also be highlighted. Other topics for consideration include studies of tissue-specific adult stem cells; signaling mechanisms for the inhibition of fibrosis and inflammation related to the promotion of normal tissue repair; epithelial-mesenchymal-transformation (EMT) for tissue repair; and signaling in vertebrate limb regeneration. I encourage you to submit a manuscript to this issue dedicated to the exploration of current research in the tissue repair field.
Dr. Regina M. Day
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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a 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 monthly journal published by MDPI.
- tissue repair
- signaling pathways
- adult stem cells
- pluripotent cell reprogramming
- growth factor regulation for tissue repair
- cellular proliferation for tissue repair
- cell migration for tissue repair
- wound microenvironment
- injury-induced inflammation
- epithelial-mesenchymal transformation
- mesenchymal-epithelial transformation