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.

Adult stem cells are responsible for tissue regeneration and repair throughout life. Their quiescence or activation are tightly regulated by common signalling pathways that often recapitulate those happening during embryonic development, and thus it is important to understand their regulation not only in postnatal life, but also during foetal development. In this regard, skeletal muscle is an interesting tissue since it accounts for a large percentage of body mass (about 40%), it is highly amenable to intervention through exercise and it is also key in metabolic and physiological changes underlying frailty susceptibility in the elderly. While muscle-resident satellite cells are responsible for all myogenic activity in physiological conditions and become senescent in old age, other progenitor cells such as mesoangioblasts do seem to contribute to muscle regeneration and repair after tissue damage. Similarly, fibro-adipogenic precursor cells seem to be key in the aberrant response that fills up the space left from atrophied muscle mass and which ends up with a dysfunctional muscle having vast areas of fatty infiltration and fibrosis. The complex interplay between these stem/progenitor cell types and their niches in normal and pathological conditions throughout life are the subjects of intense investigation. This eBook highlights recent developments on the role of stem cells in skeletal muscle function, both in prenatal and postnatal life, and their regulation by transcriptional, post-transcriptional and epigenetic mechanisms. Additionally, it includes articles on interventions associated with exercise, pathological changes in neuromuscular diseases, and stem cell aging.

A healthy skeletal musculature is necessary for a good quality of life and is important in sports. The loss of skeletal muscle mass leads to severe clinical complications and alters daily functioning. The aim of this book is to give an overview of skeletal muscle atrophy including pathomechanism, clinical characters, and the tools for prevention and treatment. Skeletal muscle atrophy can develop due to neurogenic or myogenic reasons, and frequently appears as an age-dependent disorder (sarcopenia). The studies of theoretical background give promising perspectives to prevent and treat muscle atrophy. The book is recommended to scientists, practitioners, students, sportsmen, and everybody who is interested in the normal and impaired function of the skeletal muscle.

This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.

This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.

The World Health Organization Organization estimates that over 1.9 billion people worldwide are now obese or overweight [body mass index (BMI) > 27 Kg/m2]. Type 2 diabetes (T2D) is now recognized as the most devastating complications of obesity. Intimate relationship exists between obesity, innate (neutrophils, dendritic cells, macrophages, mast cells, and eosinophils) and adaptive (B and T lymphocytes) immune cells. Cells of the innate immune system produce inflammatory cytokines, and other factors leading to impaired insulin secretion and insulin resistance. Likewise, B lymphocytes (mostly B2 cells) are activated in obese adipose tissue and contribute to proinflammatory activation of adipose tissue macrophages and T cells resulting in insulin resistance. Thus, obesity-induced low-grade inflammation in adipose tissue, liver, skeletal muscle, and pancreas not only activates the innate and adaptive systems affecting metabolic homeostasis, it also results in fibrosis and necrosis. It is now becoming increasingly evident that fibrosis is a major contributor to metabolic dysregulation in obese and T2D patients and that advanced liver fibrosis leads to cirrhosis and death. The health risks associated with obesity are further exaggerated by smoking. This research topic consisting of 10 articles (9 reviews and one original) provide a comprehensive assessment of the impact of obesity on immunometabolism, cardiac functions, the connections of nicotine to NAFLD, the expression of hepatic carcinoembryonic antigen related cell adhesion molecule 1 (CEACAM1), the role chromogranin A (CgA) and its peptides pancreastatin (PST) and catestatin (CST) in insulin sensitivity, the loss of skeletal muscle mass and function, and the alternate RNA splicing.