Human Skeletal Muscle Aging & Mutagenesis
Study on the aging of human skeletal muscles, mutagenesis and the role #satellite cell.
The interplay between stem cells’ intrinsic and extrinsic components will help to improve cell therapies that can restore tissue homeostasis in older people and enhance muscle repair.
The human body is affected by aging in multiple ways. Human aging can lead to a decrease in skeletal muscles (SkM), and in the number of satellite cells (SCs), resident stem cells. To study the relationship between SC aging, and muscle impairment in healthy individuals (aged 21-78), the whole genomes of SC clones from the leg muscle vastus latis were analyzed. The rapid increase in SCs in healthy adult muscles is consistent with an accumulation rate of thirteen somatic mutations on each genome per year. SkM-expressed gene mutations are rare because they’re protected. As mutations increase in exons, promoters, and genes that are involved in SC function and muscle activity, they become targeted, resulting in aging. The exons of an RNA transcription or DNA that encodes it are the sections which are translated to protein. Proteins are a synthesis of molecules. A single base pair change that led to the substitution of another amino acid (missense mutation), which was detected in conjunction with SC mutations that affected the entire tissue. #Somatic mutations in SCs are the cause of the age-related decline in SkM function.
Satellite Cells
Satellite cells (SCs), a heterogeneous group of stem and progenitor cell types, are also known as satellite cells. These cells are important in the growth and formation of myofiber. Satellite cells play a pivotal role in the enlargement, remodeling, and regeneration of skeletal muscles (SkM). Satellite cells remain dormant up until they are activated by exercise or SkM injuries. Skeletal muscle has a remarkable capacity to recover after injury. Skeletal muscles undergo a complex degeneration and regeneration process at the cellular and molecular level. This regeneration process is dependent on the dynamic interaction between satellite cells (and their environment, stem cell niche) When committed to myogenic differentiation, SCs multiply even more. SCs multiply and combine with SkM fibers to supply new nuclei for the growing and regeneration fibers. One sign of human SkM aging is the decline in proliferative capacity of SCs.
It is predicted that a defective SC compartment will be a major factor in age-related deficiencies such as restricted skeletal muscle mobility and reduced voluntary functions. These defects can lead to a decreased ability to respond to hypertrophic stimulations such as exercise, impaired recovery after muscle injury or disuse, and disruption of tissue homeostasis. The SCs from nonactive adult mice have also been shown to contribute towards differentiated fibers within non-injured muscle. The basal turnover in nuclei of adult fibers is less important in protecting against sarcopenia. The hypothesis was tested, and it was found that a lifelong reduction in satellite cells does not accelerate or exacerbate sarcopenia. Satellite cells do not contribute to maintaining muscle size and fiber type composition as we age. However, their loss can contribute to age related muscle fibrosis. Saropenia, the progressive loss of SkM function and mass, affects as much as 29% of people aged 85. Sarcopenia can be a very disabling condition. It is important to continue exploring the role of SCs in pathology. SCs play a major role in limiting fibrosis of the SkM in mice with sarcopenia.
Up to 29% (or 85 year olds) of the population suffer from sarcopenia, a progressive loss in SkM mass and function. Sarcopenia can be a very disabling condition. It is important to continue exploring the role of SCs in pathology. Scs play a key role in limiting fibrosis within the SkM in mice with sarcopenia. The integrity of the genome is crucial for stem cells to function. There must still be some stability in the genome. Genetic mutations of the soma can have a variety of physiological and pathological effects, including the loss stem-cell function. Modifications in the genome occur throughout life, starting with the first division of embryos. They can range from single base changes (single nucleotide variations (SNVs), to insertions and deletions of several bases (indels), to chromosomal rearrangements. Somatic variants do not affect the entire individual, but rather a subpopulation within the body.
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