Nutrition and microRNAs: Novel Insights to Fight Sarcopenia

Abstract

Sarcopenia is a progressive age-related loss of skeletal muscle mass and strength, which may result in increased physical frailty and a higher risk of adverse events. Low-grade systemic inflammation, loss of muscle protein homeostasis, mitochondrial dysfunction, and reduced number and function of satellite cells seem to be the key points for the induction of muscle wasting, contributing to the pathophysiological mechanisms of sarcopenia. While a range of genetic, hormonal, and environmental factors has been reported to contribute to the onset of sarcopenia, dietary interventions targeting protein or antioxidant intake may have a positive effect in increasing muscle mass and strength, regulating protein homeostasis, oxidative reaction, and cell autophagy, thus providing a cellular lifespan extension. MicroRNAs (miRNAs) are endogenous small non-coding RNAs, which control gene expression in different tissues. In skeletal muscle, a range of miRNAs, named myomiRNAs, are involved in many physiological processes, such as growth, development, and maintenance of muscle mass and function. This review aims to present and to discuss some of the most relevant molecular mechanisms related to the pathophysiological effect of sarcopenia. Besides, we explored the role of nutrition as a possible way to counteract the loss of muscle mass and function associated with ageing, with special attention paid to nutrient-dependent miRNAs regulation. This review will provide important information to better understand sarcopenia and, thus, to facilitate research and therapeutic strategies to counteract the pathophysiological effect of ageing.

Physical frailty and long-term mortality in older people with chronic heart failure with preserved and reduced ejection fraction: a retrospective longitudinal study

“…Clinically, to define frailty, it is based on phenotypical descriptions focusing on functional manifestations of frailty involving muscle weakness, reduced exercise tolerance, walking speed, physical activity, and weight loss [11], or deficit-based descriptions including disabilities, diseases, and laboratory examinations [23]. The possible causes of muscle strength decline include an imbalance between catabolic and anabolic signaling, chronic inflammation due to environmental and psychosocial factors, genetic factors, gut microbiomes, lifestyles, exercise, and nutrition [24][25][26][27]. In our studies, among different frailty assessment tools, the Fried criteria revealed a proportion of 52.5% of patients as frail, and the Rockwood frailty assessment tool found a proportion of 79.4% as frail (Table 1).…”

Taurine Attenuates Catabolic Processes Related to the Onset of Sarcopenia

“…During aging, a chronic low-grade inflammatory state known as “inflammaging” occurs, characterized by an increased systemic concentration of proinflammatory cytokines [ 3 ]. In particular, Tumor Necrosis Factor α (TNF) and Interleukin-6 (IL-6) have been implicated in the inflammatory response in skeletal muscle, and an age-related increase of these inflammatory markers is thought to contribute to the sarcopenic phenotype [ 4 , 5 , 6 ]. Although the molecular mechanisms involved in the interaction between inflammaging and muscle loss have not yet been understood, recent findings demonstrate that the increased levels of low-grade inflammation may favor dysregulation between synthesis and protein degradation [ 2 , 7 , 8 ].…”

Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications

“…These data highlight that a long period of inactivity significantly affects satellite cell function and suggests that controlling and increasing satellite cell number during aging may represent an efficient strategy to preserve NMJ health, delaying the loss of muscle mass and function. These severe alterations of satellite cell function, which occur with advancing aging, can be the result of either extrinsic or intrinsic events such as impaired self-renewal mechanisms, exhaustion following forced differentiation, and alteration of muscle environment [ 158 , 159 , 160 ]. In 2005, heterochronic transplantation experiments performed in the Conboy laboratory demonstrated that aged satellite cells exposed to a young systemic environment showed dramatic improvements in functionality [ 161 ].…”