Muscle Homeostasis And Regeneration

The book is a collection of original research and review articles addressing the intriguing field of the cellular and molecular players involved in muscle homeostasis and regeneration. One of the most ambitious aspirations of modern medical science is the possibility of regenerating any damaged part of the body, including skeletal muscle. This desire has prompted clinicians and researchers to search for innovative technologies aimed at replacing organs and tissues that are compromised. In this context, the papers, collected in this book, addressing a specific aspects of muscle homeostasis and regeneration under physiopathologic conditions, will help us to better understand the underlying mechanisms of muscle healing and will help to design more appropriate therapeutic approaches to improve muscle regeneration and to counteract muscle diseases.

The book is a collection of original research and review articles addressing the intriguing field of the cellular and molecular players involved in muscle homeostasis and regeneration. One of the most ambitious aspirations of modern medical science is the possibility of regenerating any damaged part of the body, including skeletal muscle. This desire has prompted clinicians and researchers to search for innovative technologies aimed at replacing organs and tissues that are compromised. In this context, the papers, collected in this book, addressing a specific aspects of muscle homeostasis and regeneration under physiopathologic conditions, will help us to better understand the underlying mechanisms of muscle healing and will help to design more appropriate therapeutic approaches to improve muscle regeneration and to counteract muscle diseases.

Homeostasis refers to the ability of an organism to keep the body's internal environment within bounds that enable the organism to survive. Chemical regulation, thermoregulation and osmoregulation are the primary types of homeostatic regulations that occur in the body. Muscle regeneration is the ability of an adult muscle to regenerate damaged fibers and it represents an essential homeostatic function. It is an extremely coordinated program, which partly mimics the embryonic developmental program. It also includes the activation of the muscle compartment of stem cells, specifically satellite cells as well as other precursor cells. The activities of these cells are dependent on environmental signals. Muscle regeneration can be hampered by a number of pathological conditions either because of the increasing loss of stem cell populations or due to the absence of signals that prevent damaged tissues from effectively activating a regenerative program. Thus, it is possible that losing control over these cells will result in pathological cell differentiation. The topics included herein on muscle regeneration and homeostasis is of utmost significance and bound to provide incredible insights to readers. Those in search of information to further their knowledge will be greatly assisted by this book.

The search for knowledge on cellular and molecular mechanisms involved in skeletal muscle mass homeostasis and regeneration is an exciting scientific area and extremely important to develop therapeutic strategies for neuromuscular disorders and conditions related to muscle wasting. The mechanisms involved in the regulation of skeletal muscle mass and regeneration consist of molecular signaling pathways modulating protein synthesis and degradation, bioenergetics alterations and preserved function of muscle stem cells. In the last years, different kinds of stem cells has been reported to be localized into skeletal muscle (satellite cells, mesoangioblasts, progenitor interstitial cells and others) or migrate from non-muscle sites, such as bone marrow, to muscle tissue in response to injury. In addition, myogenic progenitor cells are also activated in skeletal muscle wasting disorders. The goal of this research topic is to highlight the available knowledge regarding skeletal muscle and stem cell biology in the context of both physiological and pathological conditions. Our purpose herein is to facilitate better dissemination of research into skeletal muscle physiology field. Frontiers in Physiology is a journal indexed in: PubMed Central, Scopus, Google Scholar, DOAJ, CrossRef.

The search for knowledge on cellular and molecular mechanisms involved in skeletal muscle mass homeostasis and regeneration is an exciting scientific area and extremely important to develop therapeutic strategies for neuromuscular disorders and conditions related to muscle wasting. The mechanisms involved in the regulation of skeletal muscle mass and regeneration consist of molecular signaling pathways modulating protein synthesis and degradation, bioenergetics alterations and preserved function of muscle stem cells. In the last years, different kinds of stem cells has been reported to be localized into skeletal muscle (satellite cells, mesoangioblasts, progenitor interstitial cells and others) or migrate from non-muscle sites, such as bone marrow, to muscle tissue in response to injury. In addition, myogenic progenitor cells are also activated in skeletal muscle wasting disorders. The goal of this research topic is to highlight the available knowledge regarding skeletal muscle and stem cell biology in the context of both physiological and pathological conditions. Our purpose herein is to facilitate better dissemination of research into skeletal muscle physiology field.

Since the middle of the last century we have progressively built up a comprehensive descriptive model of the allied mechanisms that maintain our muscles at a size and strength appropriate to the functional demands upon them and that rapidly repair damaged muscles. This volume is an assemblage of the collective experience from the pick of major research groups investigating these aspects of muscle cell biology. It provides up-to-date coverage and presents a broad range of topics.

A version of the OpenStax text

"Skeletal muscle is one of the most dynamic human tissues and it is critical for the voluntary movement of the body. Muscle function is tightly linked to its delicate structure, which is mainly composed of myofibers and connective tissues. Muscle contraction is achieved by the cooperation of diverse types of myofibers, and supported by muscle metabolism that is dependent on robust mitochondria activity. When homeostasis is disrupted, skeletal muscle exhibits various strategies to deal with the injury, depending on the severity of the injury. Muscle regeneration has strong links with the activation of a muscle stem cell transcriptional program. CCCTC-binding factor (CTCF) is an indispensable protein in vertebrates and promotes a myogenic differentiation program in muscle cell line. It is regarded as a multifunctional epigenetic regulatory protein. CTCF was first identified as a transcriptional repressor. In addition to the regulation of transcription, it also plays a critical role as a genomic architectural protein. Recent studies indicate that CTCF is involved in muscle-related diseases. However, the role of CTCF in skeletal muscle in vivo homeostasis has not been explored. Our novel study investigated whether CTCF plays a role in skeletal muscle formation and function through employing a Ctcf knockout mouse, HSACre/+; Ctcffl/fl mice. In this model, Ctcf expression is specifically reduced in skeletal muscle myonuclei, starting at 9.5 days post coitum. We found that these mice started to progressively lose weight and muscle mass at 8 weeks after birth, and demonstrated dramatic muscle wasting by 13 weeks. Meanwhile, CTCF-deficient mice also exhibit serious defects in muscle function and contraction. Furthermore, the loss of CTCF in skeletal muscles lead to signs of regeneration at 13 weeks, while these muscles only had a few degenerating myofibers. It suggests that CTCF-deficient muscle may suffer from continuous muscle injuries which trigger strong muscle regeneration. Transcriptome analysis provides insight that repression of genes involved in muscle contraction and homeostasis may underlie the muscle wasting observed in Ctcf knockout mice"--