In the past few decades, obesity in the pediatric population has dramatically increased and is common in many countries. Childhood obesity often causes health problems and increases the risk of cardiometabolic diseases such as type 2 diabetes, nonalcohol fatty liver, and cardiovascular diseases. Obesity in young people has been closely associated with environmental, behavioral, and genetic defects, including the availability of high-energy and sugary food and beverages, sedentary behavior, and hereditary factors. Few drugs are currently available to treat obesity in children and adolescents because it is difficult to demonstrate the safety of these drugs on the growth and development of the youth. Lifestyle modifications, such as diet control and physical exercise, are the primary approaches for preventing and treating childhood obesity. Among them, physical activity is a crucial component. This review summarizes the epidemiology, cardiometabolic risk of obesity, therapeutic strategies, and the benefits of exercise on obesity-related chronic diseases in children and adolescents.

With the aging of the global population, accumulating interest is focused on manipulating the fundamental aging-related signaling pathways to delay the physiological aging process and eventually slow or prevent the appearance or severity of multiple aging-related diseases. Recently, emerging evidence has shown that RNA modifications, which were historically considered infrastructural features of cellular RNAs, are dynamically regulated across most of the RNA species in cells and thereby critically involved in major biological processes, including cellular senescence and aging. In this review, we summarize the current knowledge about RNA modifications and provide a catalog of RNA modifications on different RNA species, including mRNAs, miRNAs, lncRNA, tRNAs, and rRNAs. Most importantly, we focus on the regulation and roles of these RNA modifications in aging-related diseases, including neurodegenerative diseases, cardiovascular diseases, cataracts, osteoporosis, and fertility decline. This would be an important step toward a better understanding of fundamental aging mechanisms and thereby facilitating the development of novel diagnostics and therapeutics for aging-related diseases.

Muscle atrophy is a frequently observed complication, characterized by the loss of muscle mass and strength, which diminishes the quality of life and survival. No effective therapy except exercise is currently available. In our previous study, repressing miR-29b has been shown to reduce muscle atrophy. In our current study, we have constructed artificially engineered extracellular vesicles for the delivery of CRISPR/Cas9 to target miR-29b (EVs-Cas9-29b). EVs-Cas9-29b has shown a favorable functional effect with respect to miR-29b repression in a specific and rapid manner by gene editing. In in vitro conditions, EVs-Cas9-29b could protect against muscle atrophy induced by dexamethasone (Dex), angiotensin II (AngII), and tumor necrosis factor-alpha (TNF-α). And EVs-Cas9-29b introduced in vivo preserved muscle function in the well-established immobilization and denervation-induced muscle atrophy mice model. Our work demonstrates an engineered extracellular vesicles delivery of the miR-29b editing system, which could be potentially used for muscle atrophy therapy.

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