Part of the book: Stem Cells in Clinic and Research
Part of the book: Skeletal Muscle
In the last decades, there has been a remarkable advance in the treatment of most types of cancer, improving the patient’s prognosis. During cancer progression, tumor cells develop several biological changes to support initiation, proliferation, and resistance to death. Nearly 50–80% of all oncologic patients experience rapid weight loss that is related to ~20% of cancer-related deaths. Cancer cachexia is a syndrome characterized by loss of skeletal muscle mass, anorexia, and anemia. A lot of effort in scientific investigation has contributed to the understanding of cancer processes, in which epigenetic changes, as microRNAs, can influence cancer progression. Therefore, useful strategies to control the cancer-induced epigenetic changes in the tumor cells can have a key role in a clinical perspective to decrease the cancer development and aggressiveness. Physical activity has been proposed as a suitable tool to manage tumor growth and cachexia and to improve the deleterious sequelae experienced during cancer treatment. Although the molecular mechanisms involved in these responses are poorly understood, this chapter aims to discuss the role of microRNAs in the cancer-induced epigenetic changes and how physical activity could influence the epigenetic control of tumor cells and cachexia and their potential role in clinical applications for cancer.
Part of the book: Epigenetics
Exercise training (ET) represents a non-pharmacological treatment that can attenuate or even reverse the process of cardiovascular diseases (CVD), by stimulating protein synthesis, angiogenesis, mitochondrial biogenesis, anti-inflammatory, and anti-oxidative effects that are involved to enhance the performance and improved quality of life. Despite the benefits of exercise, the intricacies of their underlying molecular mechanisms remain largely unknown. Noncoding RNAs (ncRNAs) have been recognized as a major regulatory network governing gene expression in several physiological processes and appeared as pivotal modulators in a myriad of cardiovascular processes under physiological and pathological conditions. However, little is known about ncRNA expression and role in response to exercise. Here we review the current understanding of the ncRNA role in exercise-induced adaptations focused on the cardiovascular system and address their potential role in clinical applications for cardiovascular diseases.
Part of the book: Muscle Cells
Sarcopenia has been defined as the loss of skeletal muscle mass and strength that occurs with advancing age and has also been related to many metabolic diseases. In late stages, sarcopenia precedes cachexia, defined as a multifactorial syndrome characterized by an ongoing skeletal muscle wasting, with or without loss of fat mass, associated with poor prognosis in diseases, worsening quality of life and survival. Heart failure and cancer-associated cachexia represents a progressive involuntary weight loss and is mainly the result of an imbalance in the muscle protein synthesis and degradation, inflammation, and oxidative stress, causing muscle wasting. Importantly, both diseases are still the main causes of death worldwide and the molecular basis of cachexia is still poorly understood. Recently, non-coding RNAs have been described to regulate the cardiac and cancer-associated cachexia. On the other hand, exercise training is a promising ally in slowing down cachexia and improving the quality of life of patients. New studies demonstrate that exercise training, acting through non-coding RNAs, may be able to mitigate muscle wasting, as protein turnover, mitochondrial biogenesis, and antioxidant capacity improvement. This review will therefore discuss the molecular mechanisms associated with the muscle wasting in both cardiac and cancer cachexia, as well as highlighting the effects of exercise training in attenuating the loss of muscle mass in these specific conditions.
Part of the book: Frailty and Sarcopenia