Insulin-like growth factor-I (IGF-1) is an important mediator in numerous developmental processes, such as proliferation, differentiation, survival, growth, apoptosis and regeneration. Mouse genetics have provided important insights into the signalling mechanisms that are necessary for the coordination of muscle repair. Recent studies on the role of IGF-1 in the promotion of cell recruitment to the injured muscle and the subsequent resolution of the inflammatory response have unveiled new perspectives into local repair mechanisms.
"In this regard , there are reports supporting the cooperation between NFAT and NF - kappa B signaling pathways in processes such as the regulation of T - cell proliferation , maturation , and acti - vation ( Macian , 2005 ) . In addition , insulin - like growth factor I ( IGF - 1 ) has multiple effects during tissue development and regen - eration , and there is evidence of NFAT activation in response to IGF - 1 stimulation in tissues such as muscle ( Mourkioti and Rosenthal , 2005 ; Valdes et al . , 2013 ) . "
"Therefore, interventions that focus on the IGF-1/mTOR pathway will also induce activation of the support-system for addition of myonuclei. IGF-1 acts both intracellularly and extracellularly to induce both proliferation and differentiation of SCs (Bischoff, 1986; Adams and Haddad, 1996; Adams, 1998; Cameron-Smith, 2002; Mourkioti and Rosenthal, 2005) and different isoforms of IGF-1 may be responsible for these (see Review for further reading of the IGF-1 and skeletal muscle regeneration and hypertrophy: Philippou et al., 2007). mTOR has been described as the master regulator of cellular processes and has been linked to differentiation in C2C12 myobalsts (Erbay et al., 2003; Han et al., 2008). "
[Show abstract][Hide abstract] ABSTRACT: Maintenance of skeletal muscle is essential for health and survival. There are marked losses of skeletal muscle mass as well as strength and physiological function under conditions of low mechanical load, such as space flight, as well as ground based models such as bed rest, immobilization, disuse, and various animal models. Disuse atrophy is caused by mechanical unloading of muscle and this leads to reduced muscle mass without fiber attrition. Skeletal muscle stem cells (satellite cells) and myonuclei are integrally involved in skeletal muscle responses to environmental changes that induce atrophy. Myonuclear domain size is influenced differently in fast and slow twitch muscle, but also by different models of muscle wasting, a factor that is not yet understood. Although the myonuclear domain is 3-dimensional this is rarely considered. Apoptosis as a mechanism for myonuclear loss with atrophy is controversial, whereas cell death of satellite cells has not been considered. Molecular signals such as myostatin/SMAD pathway, MAFbx, and MuRF1 E3 ligases of the ubiquitin proteasome pathway and IGF1-AKT-mTOR pathway are 3 distinctly different contributors to skeletal muscle protein adaptation to disuse. Molecular signaling pathways activated in muscle fibers by disuse are rarely considered within satellite cells themselves despite similar exposure to unloading or low mechanical load. These molecular pathways interact with each other during atrophy and also when various interventions are applied that could alleviate atrophy. Re-applying mechanical load is an obvious method to restore muscle mass, however how nutrient supplementation (e.g., amino acids) may further enhance recovery (or reduce atrophy despite unloading or ageing) is currently of great interest. Satellite cells are particularly responsive to myostatin and to growth factors. Recently, the hibernating squirrel has been identified as an innovative model to study resistance to atrophy.
Frontiers in Physiology 03/2014; 5:99. DOI:10.3389/fphys.2014.00099 · 3.53 Impact Factor
"These alterations lead to adverse manifestations, such as accumulation of fat deposits in bone and muscles, impaired healing and fibrosis after severe injury, or altered hematopoiesis and autoimmunity (Lepperdinger, 2011). Among the mechanisms involved in this process, insulin, IGF- 1, mTOR and leptin signalling pathways hardwire the link between nutrition and aging related processes, and mediate the endocrine derangements that characterize obesity, metabolic syndrome and diabetes mellitus (Mourkioti and Rosenthal, 2005). "
[Show abstract][Hide abstract] ABSTRACT: Adult tissue stem cells have the ability to adjust to environmental changes and affect also the proliferation of neighboring cells, with important consequences on tissue maintenance and regeneration. Stem cell renewal and proliferation is strongly regulated during aging of the organism. Caloric restriction is the most powerful anti-aging strategy conserved throughout evolution in the animal kingdom. Recent studies relate the properties of caloric restriction to its ability in reprogramming stem-like cell states and in prolonging the capacity of stem cells to self-renew, proliferate, differentiate, and replace cells in several adult tissues. However this general paradigm presents with exceptions. The scope of this review is to highlight how caloric restriction impacts on diverse stem cell compartments and, by doing so, might differentially delay aging in the tissues of lower and higher organisms.
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