Skeletal muscle is one of the leading frameworks of the musculo-skeletal system, which works in synergy with the bones. Long skeletal muscles provide stability and mobility to the human body and are primarily composed of proteins. Conversely, improper functioning of various skeletal muscles leads to diseases and disorders, namely, age-related muscle disorder called sarcopenia, a group of genetic muscle disorders such as muscular dystrophies, and severe muscle wasting in cancer known as cachexia. However, skeletal muscle has an excellent ability to undergo hypertrophy and enhanced functioning during sustained exercise over time. Indeed, these processes of skeletal muscle regeneration/hypertrophy, as well as degeneration and atrophy, involve an interplay of various signaling pathways. Myostatin is one such chemokine/myokine with a significant contribution to muscle regeneration or atrophy in multiple conditions. In this review, we try to put together the role and regulation of myostatin as a function of muscle regeneration extrapolated to multiple aspects of its molecular functions.
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http://dx.doi.org/10.1016/j.afos.2023.03.008 | DOI Listing |
Curr Cardiol Rep
January 2025
Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, 1470 Madison Avenue, New York, NY, 10029, USA.
Purpose Of The Review: This review aims to discuss the process of cardiomyocyte maturation, with a focus on the underlying molecular mechanisms required to form a fully functional heart. We examine both long-standing concepts associated with cardiac maturation and recent developments, and the overall complexity of molecularly integrating all the processes that lead to a mature heart.
Recent Findings: Cardiac maturation, defined here as the sequential changes that occurring before the heart reaches full maturity, has been a subject of investigation for decades.
J Pediatr Ophthalmol Strabismus
January 2025
Purpose: To investigate the effects of recession or re-section surgery on PAX 7 positive satellite cells of the extraocular muscle (EOM) in rabbits.
Methods: A total of 20 rabbits (40 eyes) were included in this study. The superior rectus muscle of the right eye was either recessed or resected.
Front Cell Neurosci
January 2025
Laboratório de Neurodegeneração e Reparo - Departamento de Anatomia Patológica, Hospital Universitário Clementino Fraga Filho, HUCFF/UFRJ, Rio de Janeiro, Brazil.
Background: Following transection, nerve repair using the polylactic acid (PLA) conduit is an effective option. In addition, inosine treatment has shown potential to promote nerve regeneration. Therefore, this study aimed to investigate the regenerative potential of inosine after nerve transection and polylactic acid conduit repair.
View Article and Find Full Text PDFERJ Open Res
January 2025
Faculty of Health and Life Sciences, Northumbria University Newcastle, Newcastle upon Tyne, UK.
Background: In response to exercise-based pulmonary rehabilitation (PR), the type of muscle fibre remodelling differs between COPD patients with peripheral muscle wasting (atrophic patients with COPD) and those without wasting (nonatrophic patients with COPD). Extracellular matrix (ECM) proteins are major constituents of the cell micro-environment steering cell behaviour and regeneration. We investigated whether the composition of ECM in atrophic compared to nonatrophic patients with COPD differs in response to PR.
View Article and Find Full Text PDFFront Cell Dev Biol
January 2025
Department of Human Genetics, Leiden University Medical Center (LUMC), Leiden, Netherlands.
Muscle repair and regeneration are complex processes. In Duchenne muscular dystrophy (DMD), these processes are disrupted by the loss of functional dystrophin, a key part of the transmembrane dystrophin-associated glycoprotein complex that stabilizes myofibers, indirectly leading to progressive muscle wasting, subsequent loss of ambulation, respiratory and cardiac insufficiency, and premature death. As part of the DMD pathology, histone deacetylase (HDAC) activity is constitutively increased, leading to epigenetic changes and inhibition of muscle regeneration factors, chronic inflammation, fibrosis, and adipogenesis.
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