OBM Genetics is an international Open Access journal published quarterly online by LIDSEN Publishing Inc. It accepts papers addressing basic and medical aspects of genetics and epigenetics and also ethical, legal and social issues. Coverage includes clinical, developmental, diagnostic, evolutionary, genomic, mitochondrial, molecular, oncological, population and reproductive aspects. It publishes research articles, reviews, communications and technical notes, 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.
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Publication Speed (median values for papers published in 2022): Submission to First Decision: 4 weeks; Submission to Acceptance: 12 weeks; Acceptance to Publication: 13 days (1-2 days of FREE language polishing included)
Molecular Mechanisms of Skeletal Muscle Wasting and Weakness in Different Pathophysiological Conditions
Submission Deadline: May 31, 2022 (Open) Submit Now
Junaith S. Mohamed, PhD, Assistant Professor
Laboratory of Muscle and Nerve, Department of Diagnostic and Health Sciences, Division of Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, TN 38163, USA
Research interests: aging; post-stroke muscle morbidities; muscle atrophy; growth and regeneration; genomics; proteomics; metabolomics
About This Topic
Skeletal muscle is the largest organ in the human body comprising ~40% of the total body weight. Maintenance of muscle mass and function is critical for health. Since skeletal muscle is one of the major metabolic tissues in our body, maintaining muscle mass and function is also vital for preventing metabolic disorders. Chronic diseases such as stroke, cancer, cardiovascular, sepsis, tuberculosis, and AIDS will often result in severe muscle wasting leading to drug intolerance that subsequently causes mobility, and mortality. While aging is a natural process, one of the hallmarks of aging is the loss of muscle mass and strength, a condition called sarcopenia. Muscle wasting is caused as a result of low muscle protein synthesis and accelerated muscle protein degradation. The molecular origin of muscle wasting in response to different pathophysiological settings are poorly studied. Moreover, skeletal muscles are post-mitotically quiescent therefore muscle repair and growth rely on muscle stem-cells called satellite cells. Once the satellite cells are activated upon intrinsic and/or extrinsic stimuli, they undergo remarkable proliferation. The proliferating satellite cells are subsequently differentiated into and/or fuse with existing muscle fibers. Therefore, both the quality and quantity of satellite cells critical to prevent muscle loss. Understanding the molecular and cellular mechanisms of muscle wasting will identify potential therapeutic targets that will open a new avenue for the treatment of muscle wasting in various disease/disorder conditions. This Special Issue covers topics related to skeletal muscle wasting and weakness in both human and animal models. Authors interested in contributing their research findings to this Special Issue are invited to provide a tentative title and author details to the Guest Editor, with the submission of full articles no later than October 31, 2021. Manuscripts will be subject to peer review according to the standard procedures of OBM Genetics. Upon manuscript submission, please indicate that your manuscript has prepared for the Special Issue “Molecular Mechanisms of Skeletal Muscle Wasting and Weakness in Different Pathophysiological Conditions.”
Received: 28 March 2023; Published: 19 September 2023; doi: 10.21926/obm.genet.2303192
Human skeletal muscle exhibits remarkable plasticity, being responsive to chemical, mechanical, metabolic, and inflammatory stress. When the homeostatic disturbance is below a threshold of significant damage, the muscle responds by modifying metabolic activity, cell size/shape, and structure, thereby normalizing cellular function. If the distu [...]
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