OBM Geriatrics is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. The journal takes the premise that innovative approaches – including gene therapy, cell therapy, and epigenetic modulation – will result in clinical interventions that alter the fundamental pathology and the clinical course of age-related human diseases. We will give strong preference to papers that emphasize an alteration (or a potential alteration) in the fundamental disease course of Alzheimer’s disease, vascular aging diseases, osteoarthritis, osteoporosis, skin aging, immune senescence, and other age-related diseases.

Geriatric medicine is now entering a unique point in history, where the focus will no longer be on palliative, ameliorative, or social aspects of care for age-related disease, but will be capable of stopping, preventing, and reversing major disease constellations that have heretofore been entirely resistant to interventions based on “small molecular” pharmacological approaches. With the changing emphasis from genetic to epigenetic understandings of pathology (including telomere biology), with the use of gene delivery systems (including viral delivery systems), and with the use of cell-based therapies (including stem cell therapies), a fatalistic view of age-related disease is no longer a reasonable clinical default nor an appropriate clinical research paradigm.

Precedence will be given to papers describing fundamental interventions, including interventions that affect cell senescence, patterns of gene expression, telomere biology, stem cell biology, and other innovative, 21st century interventions, especially if the focus is on clinical applications, ongoing clinical trials, or animal trials preparatory to phase 1 human clinical trials.

Papers must be clear and concise, but detailed data is strongly encouraged. The journal publishes a variety of article types (Original Research, Review, Communication, Opinion, Comment, Conference Report, Technical Note, Book Review, etc.). There is no restriction on the length of the papers and we encourage scientists to publish their results in as much detail as possible.

Publication Speed (median values for papers published in 2023): Submission to First Decision: 5.7 weeks; Submission to Acceptance: 17.9 weeks; Acceptance to Publication: 7 days (1-2 days of FREE language polishing included)

Current Issue: 2024  Archive: 2023 2022 2021 2020 2019 2018 2017

Special Issue

Skeletal Muscle Atrophy, Growth and Repair in Different Disease and Disorder Settings

Submission Deadline: July 15, 2025 (Open) Submit Now

Guest Editor

Junaith S. Mohamed, PhD, Assistant Professor

Department of Diagnostic and Health Sciences, College of Health Professions, The University of Tennessee Health Science Center, 930 Madison Ave Suit 674, Memphis, TN 38163, USA

Website | E-Mail

Research Interests: Cerebral ischemic stroke; Skeletal muscle regeneration; Skeletal muscle metabolic disorders

About This Topic

Skeletal muscle, which makes up 40% of the body's weight, serves a variety of purposes, including preserving posture and generating movement. Since skeletal muscle involves the metabolism of both glucose and fatty acids, it is also crucial for preserving the body's overall energy homeostasis. Aging causes both quantitative and qualitative decline in muscle tissue, which raises the risk of metabolic disorders, falls, and osteoporosis. Keeping your muscle mass up will help you live a healthy life. By maintaining a balance between anabolic and catabolic processes, muscle mass is preserved. The amount of muscle will change if one of these activities is changed. For instance, more anabolic activities result in an increase in muscle mass whereas more catabolic activities induce a loss of muscle mass (muscle atrophy or wasting). Mammalian skeletal muscle also exhibits a remarkable capacity for self-regeneration on a daily basis as well as in response to myogenic stimuli like exercise, muscle growth, damage, or other myogenic factors. Through myogenesis, which is dependent on satellite cells, which are muscle stem cells, skeletal muscle regeneration and repair take place. Any dysregulation in the myogenic pathway causes poor muscle repair, which eventually led to loss of muscle mass. To cure a variety of inherited and acquired degenerative muscle illnesses and to prevent the loss of muscle mass in many catabolic circumstances, it is imperative to understand the principles of myogenesis. Understanding the mechanisms of muscle atrophy, growth and repair at the molecular level will advance clinical research and continues to guide for treatment. This special issue covers topics related to muscle atrophy, growth and repair from human and animal models. Authors interested in contributing their research findings in this special issue are invited to submit the manuscript before 15 July 2025. Manuscripts will be peer-reviewed following the standard of the journal procedures. Upon manuscript submission, please indicate that your manuscript is prepared for the special issue on "Skeletal Muscle Atrophy, Growth and Repair in Different Disease and Disorder Settings".

Keywords

Skeletal muscle; Muscle atrophy/wasting; Muscle regeneration/repair; Myogenesis; Satellite Cells; Differentiation; Sarcopenia; Cachexia; Muscular dystrophy; Muscle disorders

Manuscript Submission Information

Manuscripts should be submitted through the LIDSEN Submission System. Detailed information on manuscript preparation and submission is available in the Instructions for Authors. All submitted articles will be thoroughly refereed through a single-blind peer-review process and will be processed following the Editorial Process and Quality Control policy. Upon acceptance, the article will be immediately published in a regular issue of the journal and will be listed together on the special issue website, with a label that the article belongs to the Special Issue. LIDSEN distributes articles under the Creative Commons Attribution (CC BY 4.0) License in an open-access model. The authors own the copyright to the article, and the article can be free to access, distribute, and reuse provided that the original work is correctly cited.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). Research articles and review articles are highly invited. Authors are encouraged to send the tentative title and abstract of the planned paper to the Editorial Office (geriatrics@lidsen.com) for record. If you have any questions, please do not hesitate to contact the Editorial Office.

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