Cellular mechanisms and local progenitor activation to regulate skeletal muscle mass

Abstract

Skeletal muscle hypertrophy is a result of increased load, such as functional and stretch-overload. Activation of satellite cells and proliferation, differentiation and fusion are required for hypertrophy of overloaded skeletal muscles. On the contrary, a dramatic loss of skeletal muscle mass determines atrophy settings. The epigenetic changes involved in gene regulation at DNA and chromatin level are critical for the opposing phenomena, muscle growth and atrophy. Physiological properties of skeletal muscle tissue play a fundamental role in health and disease since it is the most abundant tissue in mammals. In fact, protein synthesis and degradation are finely modulated to maintain an appropriate muscle mass. When the molecular signaling is altered muscle wasting and weakness occurred, and this happened in most common inherited and acquired disorders such as muscular dystrophies, cachexia, and age-related wasting. To date, there is no accepted treatment to improve muscle size and strength, and these conditions pose a considerable anxiety to patients as well as to public health. Several molecules, including Magic-F1, myostatin inhibitor, IGF, glucocorticoids and microRNAs are currently investigated to interfere positively in the blueprint of skeletal muscle growth and regeneration.

Alpha sarcoglycan is required for FGF-dependent myogenic progenitor cell proliferation in vitro and in vivo

“…However, upon injury to the tissue, satellite cells become activated and proliferate as MPCs. MPCs function to repair or replace damaged fibers (Cassano et al, 2009;Collins et al, 2005) and then part of the cell population returns to quiescence in order to replenish the satellite cell pool (Zammit et al, 2004). Therefore, satellite cells are considered the unipotent adult stem cells of skeletal muscle (Zammit et al, 2006).…”

Mechanisms of exercise-induced muscle damage and fatigue: Intracellular calcium accumulation

“…IGF-1 is a potent stimulating factor of myofibrillar protein synthesis via Mammalian target of rapamycin (mTOR) pathway, mitogen-activated protein kinase (MAPK) and calcineurin pathway 67) . The mechanism about mTOR and MAPK signal transduction is summarized in recent reviews 68) . Here we focus on understanding the Ca 2+ /calmodulin-dependent transcriptional pathways.…”

Papel da proteína de choque térmico 70 induzível (HSP70) na atrofia muscular e subsequente recuperação.

“…A perda de massa muscular é uma importante manifestação clínica que pode ser ocasionada por desuso, imobilização/redução de atividade, deficiência na alimentação, uso de medicamentos específicos, glicocorticóides, envelhecimento e por patologias como câncer ou diabetes (Bodine et al, 2001;Carmeli et al, 2009;Cassano et al, 2009;Jackman, Kandarian, 2004) . Essas situações levam à atrofia muscular por reduzir a síntese proteica e/ou aumentar a degradação proteica (Cao et al, 2005;Senf et al, 2008).…”

“…Essas situações levam à atrofia muscular por reduzir a síntese proteica e/ou aumentar a degradação proteica (Cao et al, 2005;Senf et al, 2008). Além disso, a atrofia muscular está associada à diminuição da capacidade funcional do músculo esquelético e aumento do risco de morbidade e/ou mortalidade (Cassano et al, 2009;Gomes et al, 2001). …”

“…Na ausência ou redução da mobilidade muscular, como por exemplo, em situações de imobilização ou longos períodos de repouso, ocorre atrofia do músculo esquelético que é caracterizada pela redução da massa muscular indicada pela diminuição da área de secção transversal das fibras musculares e, consequente diminuição da força muscular (Cassano et al, 2009;Jackman, Kandarian, 2004;Lieber, 2002;Murphy et al, 2011).…”