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Verifying A Potential Role Of Gh In The Maintenance And Regeneration Of Skeletal Muscle Precursors

547 words - 2 pages

Introduction
Rapid developments in free radical biology and molecular technology led to the acquisition of data supporting the role of oxidative stress as a major contributor to the aging process and to the pathogenesis of a number of diseases (57, 65, 70). Oxidative damage to DNA, proteins, and lipids accumulates with age and contributes to degenerative diseases and the aging phenomenon by disrupting cellular homeostasis (1, 3, 4, 27). At the cellular level, oxidative stress generated by reactive oxygen species (ROS) and ROS-modified molecules can influence a wide range of cellular functions, leading to uncontrolled cell proliferation or accelerated cell death (20). Apoptosis also knows as programmed cell death, even though considered very important in all stage of an organism’s development, is controversially linked to the aging process. Many studies conducted on myoblasts have demonstrated that apoptosis plays an important role in skeletal muscle development by controlling the size of this population of proliferating cells which undergo differentiation into mature myotubes (31, 53, 66). Recently, consistent evidences showed that apoptosis could be a mechanism responsible of accelerated satellite cells depletion in skeletal muscle with normal aging (16, 36). Age-associated increases in apoptosis have been observed in several physiological systems, including the human immune system, human hair follicle, and rat skeletal muscle (2, 5, 59). In particular, mammalian muscle and myoblastic cells were also shown preferentially undergo to apoptosis in response to toxic agents and oxidative stress, respectively (21, 60). Programmed cell death, therefore, may be an important mechanism by which myogenic satellite cells die in response to specific stress, leading to a decrease in the regenerative capacity of...

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