Summary
The first article by Ying Wang, Michelle Wehling‐Henricks, Giuseppina Samengo & James G. Tidball describes about the aging of muscle cells and how the increase of M2a macrophages and fibrosis in aging are influenced by bone marrow aging. The aging of muscles in myeloid cells phenotype is associated with the changes in cell which may result in age-related changes in muscle structure. The aging muscles undergoes a shift in balance between myogenic potential and fibrogenic activity therefore, the muscle suffers and the capacity to repair and regenerate reduces as it becomes increasingly fibrotic. Although aged satellite cells or fibro‐adipogenic precursor (FAPs) cells also promote fibrosis, transgene expression had no effect on the expression of key signaling molecules. This article does not only tell about muscle growth but also enlightens us about the studies of the response of muscle to injury by toxin injection, the amplified, profibrotic inflammatory response in injured or diseased muscle and skeletal muscle aging too. As a result, the aging of hematopoietic compartment is accompanied by an increase in the numbers of CD163+ M2a macrophages in skeletal muscle and show that the shift toward greater numbers of M2a macrophages is associated with increased muscle fibrosis. Hence, it proves to be a very useful article for me which gives us the knowledge the muscle growth in detail.
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The second article by A. L. Rodríguez‐Perea, E. D. Arcia, C.M. Reuda & P. A. Velilla provides us information about the Phenotypical characterization of regulatory T cells in humans. Regulatory T cells consists of a fascinating subpopulation of CD4+ T cells because of their ability to limit the immune response against self and non‐self-antigens.Treg can be divided into two groups according to their site of origin: thymus‐derived (tTreg) and peripherally derived (pTreg). This article also draws our attention to the drawbacks of those markers used in chronic states of inflammation. As it can be concluded that those markers did not allow accurate representation of the Treg population or distinguish between tTreg and pTreg. The heterogeneous nature of Treg highlights the different ways to turn off the immune response of Tcons and dendritic cells, such as cell‐to‐cell contact, metabolic disturbance of the microenvironment and release of immunosuppressive cytokine. This article uses the expression of CD25, FoxP3 and CD127 to identify human Tregs. And as a result, many antibodies were used to identify the Treg populations, using the differential expression of markers, which could be mediating functional advantages. The role of treg cells in muscle regeneration is very well explained in this article. Hence, I preferred to go through it.
The third article by Bossola Maurizi, Marzetti, Emanuele, Rosa Fausto & Pacelli Fabio is about the Skeletal muscle regeneration in cancer cachexia. As the aging of muscle cells and importance of Treg cells in muscle regeneration were covered in last two articles, the third article was chosen to give some information about muscle cells in case of diseases. The article says that the wastage of muscle is the most important phenotypic and the clinical feature of cancer cachexia, and it furthers tells that the principal cause of impaired physical function, fatigue and respiratory complications. The loss of muscle has been attributed to a variable combination of reduced nutritional intake and an imbalance between catabolic and anabolic processes. It was suggested that defective muscle regeneration may also give rise to muscle wasting in cancer patients. This article gives the view of the possible therapeutic implications too. It states that the strategies currently available for the prevention and treatment of CC have proven to be only partially effective at best. The b-adrenergic signalling pathway represented to be an important therapeutic target for skeletal muscle wasting because of its role in the modulation of the mechanisms which controlled protein synthesis and degradation, as well as in the regulation of fibre type. However, the data obtained is limited, but the knowledge may be contributed to the development of therapeutic strategies to counteract the muscle wasting that occurs in cancer patients. As the article covers the very important role of skeletal muscles in cancer cachexia, it made me excited to learn more about it. Therefore, I chose it!
The fourth article by García-Prat L,Sousa-Victor P and Muñoz-Canoves P describes about the organism’s aging which is associated with the functional decline of tissues and organs and also a great decline in regenerative capacity of stem cells. The functional dysregulation of stem cells during aging is a kind of focus on skeletal muscle stem cells. The article comprises the description of stem cell aging, senescence and apoptosis, DNA damage and repair, epigenetic alterations, telomere shortening and last but not the least, a conclusion. Tissue homeostasis depends on adult stem cells. The loss of stem cell functions in the hallmark of aging which can come out as defect in self renewal ability and sometimes results in the impairment of generation. Adult skeletal muscles are made up of myofibers. The age associated change may be the central mechanisms of aging and aging‐related diseases. In the age relating, we can find the proliferation in injury and after the heterografting, there can be seen no proliferation and the injury becomes non efficient. The changes related to age in DNA methylation have revealed a complex set of
epigenetic patterns. There are so many modifications seen in aged satellite cells and specifically the environmental changes have impact on these cells. In the conclusion, we configure that with the age of organism, the tissues deteriorate slowly and the decline in stem cells functioning starts which leads to dysfunction of tissues and therefore, to more deterioration.
The fifth article by Paulsen, Goran Ramer Mikkelsen, Ulla Raastad, Truls Peake, & Jonathan M. states that induced exercise muscle damage is very important in exercise physiology. The role of leucocytes, cytokines and satellite cells in the muscle damage and regeneration is explained in this article in a very detailed manner. The article defines the exercise and induced muscle damage, changes in muscle function, the cytokine response to induced muscle damage and the response of satellite cells to eccentric exercise. Generally, the regular exercise makes our muscle stronger and more resistant to fatigue. There are several kinds of eccentric exercises which leads to muscle damage. It may occur even after the long distance running or by lifting weights. The myofibrillar disruptions indicate damage or remodelling is still not clear and debatable. According to the findings, myofibrillar changes were observed to be recovery and termed as remodelling whereas. Minor disruptions can occur without any particular changes in the force generating capacity. It is considered that the changes in muscle function reflects the extent of muscle damage. To access it directly, histological analysis of muscle tissue is required. The results of change in force generating capacity were came to be known as the subjects those who recover their force-generating capacity within 48 hours are represented as mild exercise-induced muscle damage (34 subjects). Those who recover between 2 and 7 days are presented as moderate exercise-induced muscle damage (17 subjects). Finally, subjects that do not recover within one week are presented as severe exercise-induced muscle dam- age (21 subjects). Muscle samples from severe exercise-induced that muscle damage might show a long-lasting regeneration process between 1 and 3 weeks after exercise. Therefore, it concludes that muscle damage is dependent on the type of exercise protocol. Exercise brings about systemic and local cytokine responses in skeletal muscle. The role of cytokines is not much known in regulating inflammatory responses. The examination whether cytokines are a cause or a by-product of exercise-induced muscle damage needs the relation between the responses of cytokines and markers of muscle damage. In the final part, the description of satellite cells is provided. In the conclusion, the satellite cells are undeniably needed for regeneration of muscle damage in which the parts or segments of myofibers are lost.
References
Bossola, M., Marzetti, E., Rosa, F., & Pacelli, F. (2016). Skeletal muscle regeneration in cancer cachexia. Clinical & Experimental Pharmacology & Physiology, 43(5), 522–527.Retrieved from http://search.ebscohost.com/login.aspx?direct=true&db=s3h&AN=114438092&site=eds-live&scope=site
García-Prat, L., Sousa-Victor, P., & Muñoz-Cánoves, P. (2013). Functional dysregulation of stem cells during aging: a focus on skeletal muscle stem cells. The FEBS Journal, 280(17), 4051–4062. https://doi.org/10.1111/febs.12221
Paulsen, G., Ramer Mikkelsen, U., Raastad, T., & Peake, J. M. (2012). Leucocytes, cytokines and satellite cells: what role do they play in muscle damage and regeneration following eccentric exercise? Exercise Immunology Review, 18, 42. Retrieved from http://search.ebscohost.com/login.aspx?direct=true&db=edo&AN=84343883&site=eds-live&scope=site
Rodríguez-Perea, A. L., Arcia, E. D., Rueda, C. M., & Velilla, P. A. (2016). Phenotypical characterization of regulatory T cells in humans and rodents. Clinical And Experimental Immunology, 185(3), 281–291. https://doi.org/10.1111/cei.12804
Wang, Y., Wehling-Henricks, M., Samengo, G., & Tidball, J. G. (2015). Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle-derived nitric oxide. Aging Cell, 14(4), 678–688. https://doi.org/10.1111/acel.12350
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