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      Regenerative Medicine Research: an open access translational medicine journal

      Regenerative Medicine Research
      BioMed Central

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          Abstract

          I am, as an Editor-in-Chief joining BioMed Central, so excited to announce the launch of a new biomedical journal, Regenerative Medicine Research. In this open access, online journal, we aim to publish research relating to both the fundamental and practical aspects of regenerative medicine, with a particular emphasis on translational research. Regenerative medicine is an emerging field with the potential to empower medical research and practice. The process of tissue regeneration is essential to many organisms for a healthy life, from the highly studied axolotl, to us as human beings. In many ways regenerative medicine has become the leading edge of biomedical research and clinical practice, due to its key implications for the treatment of increasingly prevalent diseases, such as heart disease. The field is in the infant stage of its development but it is growing at an impressively fast pace. For instance, based on a PubMed search, there were less than 200 articles relating to regenerative medicine published in 2002, but more than 3,000 articles published in 2012. However, comprehensive information or research data on regenerative medicine cannot presently be efficiently gathered, but can only be scrutinized through a diversity of different journals in various fields. Regenerative medicine is, by current definition, the process of creating living, functional tissues to repair or replace tissue or organ function lost due to age, disease, damage, or congenital defects [1]. Obviously, this requires a multidisciplinary approach, and one that looks beyond tissue engineering and stem cells. This need calls for a comprehensive journal and therefore, the launch of Regenerative Medicine Research takes place. We hope to publish articles that shed light on the signalling pathways involved in cell/tissue regeneration, as well as those that address how biomaterials and stem cells can be adapted or integrated into the failing organ system. Two of the first articles published in the journal today focus on the effects of chronic alcohol consumption on tissue repair and regeneration; Dekeyser et al.[2] study the effect on skeletal muscle and Borrisser-Pairó et al.[3] look at levels of IGF-1 myocardial expression. In addition, Coletti et al. [4] provide a comprehensive review comparing the cellular mechanisms of skin, nerve and muscle regeneration. As an open access journal, articles accepted for publication in Regenerative Medicine Research are made rapidly available online following acceptance. This ensures efficient dissemination of information and experimental data to scientific communities and the medical practice field. Furthermore, a highly respected Editorial Board composed of internationally well-recognized experts in the field facilitates a fair, timely and rigorous peer review process. The Editorial Board, Publisher, and myself assure the authors and readers that we are committed to making Regenerative Medicine Research a preeminent platform for exchanging research protocols and experimental data in this exciting, emerging field. We look forward to receiving your high quality contributions to the journal.

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          Most cited references3

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          Chronic alcohol ingestion delays skeletal muscle regeneration following injury

          Background Chronic alcohol ingestion may cause severe biochemical and pathophysiological derangements to skeletal muscle. Unfortunately, these alcohol-induced events may also prime skeletal muscle for worsened, delayed, or possibly incomplete repair following acute injury. As alcoholics may be at increased risk for skeletal muscle injury, our goals were to identify the effects of chronic alcohol ingestion on components of skeletal muscle regeneration. To accomplish this, age- and gender-matched C57Bl/6 mice were provided normal drinking water or water that contained 20% alcohol (v/v) for 18–20 wk. Subgroups of mice were injected with a 1.2% barium chloride (BaCl2) solution into the tibialis anterior (TA) muscle to initiate degeneration and regeneration processes. Body weights and voluntary wheel running distances were recorded during the course of recovery. Muscles were harvested at 2, 7 or 14 days post-injection and assessed for markers of inflammation and oxidant stress, fiber cross-sectional areas, levels of growth and fibrotic factors, and fibrosis. Results Body weights of injured, alcohol-fed mice were reduced during the first week of recovery. These mice also ran significantly shorter distances over the two weeks following injury compared to uninjured, alcoholics. Injured TA muscles from alcohol-fed mice had increased TNFα and IL6 gene levels compared to controls 2 days after injury. Total protein oxidant stress and alterations to glutathione homeostasis were also evident at 7 and 14 days after injury. Ciliary neurotrophic factor (CNTF) induction was delayed in injured muscles from alcohol-fed mice which may explain, in part, why fiber cross-sectional area failed to normalize 14 days following injury. Gene levels of TGFβ1 were induced early following injury before normalizing in muscle from alcohol-fed mice compared to controls. However, TGFβ1 protein content was consistently elevated in injured muscle regardless of diet. Fibrosis was increased in injured, muscle from alcohol-fed mice at 7 and 14 days of recovery compared to injured controls. Conclusions Chronic alcohol ingestion appears to delay the normal regenerative response following significant skeletal muscle injury. This is evidenced by reduced cross-sectional areas of regenerated fibers, increased fibrosis, and altered temporal expression of well-described growth and fibrotic factors.
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            Restoration versus reconstruction: cellular mechanisms of skin, nerve and muscle regeneration compared

            In tissues characterized by a high turnover or following acute injury, regeneration replaces damaged cells and is involved in adaptation to external cues, leading to homeostasis of many tissues during adult life. An understanding of the mechanics underlying tissue regeneration is highly relevant to regenerative medicine-based interventions. In order to investigate the existence a leitmotif of tissue regeneration, we compared the cellular aspects of regeneration of skin, nerve and skeletal muscle, three organs characterized by different types of anatomical and functional organization. Epidermis is a stratified squamous epithelium that migrates from the edge of the wound on the underlying dermis to rebuild lost tissue. Peripheral neurons are elongated cells whose neurites are organized in bundles, within an endoneurium of connective tissue; they either die upon injury or undergo remodeling and axon regrowth. Skeletal muscle is characterized by elongated syncytial cells, i.e. muscle fibers, that can temporarily survive in broken pieces; satellite cells residing along the fibers form new fibers, which ultimately fuse with the old ones as well as with each other to restore the previous organization. Satellite cell asymmetrical division grants a reservoir of undifferentiated cells, while other stem cell populations of muscle and non-muscle origin participate in muscle renewal. Following damage, all the tissues analyzed here go through three phases: inflammation, regeneration and maturation. Another common feature is the occurrence of cellular de-differentiation and/or differentiation events, including gene transcription, which are typical of embryonic development. Nonetheless, various strategies are used by different tissues to replace their lost parts. The epidermis regenerates ex novo, whereas neurons restore their missing parts; muscle fibers use a mixed strategy, based on the regrowth of missing parts through reconstruction by means of newborn fibers. The choice of either strategy is influenced by the anatomical, physical and chemical features of the cells as well as by the extracellular matrix typical of a given tissue, which points to the existence of differential, evolutionary-based mechanisms for specific tissue regeneration. The shared, ordered sequence of steps that characterize the regeneration processes examined suggests it may be possible to model this extremely important phenomenon to reproduce multicellular organisms.
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              Insulin-like growth factor 1 myocardial expression decreases in chronic alcohol consumption

              Background Alcoholic cardiomyopathy (CMP) is one of the major complications of chronic excessive alcohol consumption. The pathogenic mechanisms implicated are diverse, inducing functional and structural changes in the myocardium. Insulin-like Growth Factor 1 (IGF-1) plays an important role in modulating the cell cycle, and helps the differentiation and proliferation of cardiac tissue inhibiting apoptosis. Experimental studies have suggested the role of IGF-1 in alcohol-induced cardiac damage. The aim of the present study was to determine the effect of chronic alcohol consumption on IGF-1 myocardial expression and to compare this expression in cases of hypertension and other cardiac diseases. Methods We studied heart samples from human organ donors: 10 healthy donors, 16 with hypertension, 23 with chronic alcohol consumption and 7 with other causes of cardiac disease. IGF-1 myocardial expression was evaluated with a specific immunohistochemistry assay using a semi-quantitative method. Results A significant decrease in IGF-1 myocardial expression was observed comparing all the cases included with control donors. This decrease in IGF-1 myocardial expression was significantly lower in the group of donors with chronic alcohol consumption compared to controls. On group evaluation according to the presence of CMP, donors with chronic alcohol consumption without CMP presented significantly lower IGF-1 expression than controls, whereas donors with chronic alcohol consumption with CMP showed a downward trend without achieving significance. Conclusions Chronic alcohol consumption significantly reduces IGF-1 myocardial expression. This decrease induced by alcohol is partially compensated in the presence of structural myocardial damage.
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                Author and article information

                Journal
                25984320
                4376332
                10.1186/2050-490X-1-1
                http://creativecommons.org/licenses/by/2.0

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