: Childhood obesity is, according to the WHO, one of the most serious challenges of the 21st century. More than 100 million children have obesity today. Globally, the prevalence of obesity and overweight tripled in the child and youth populations from the mid-1970s (about 4%) to 2016 (greater than 18%). In 2016, more than 330 million children and adolescents were affected by overweight or obesity globally. It is estimated that by 2030 nearly 30% of all children will be affected by overweight or obesity. For this reason, childhood obesity is a major public health problem worldwide.
This study summarizes and reviewed research findings related to childhood obesity and health risks. Overweight and obesity are defined as an abnormal or excessive accumulation of fat that can harm health. Obesity has a multifactorial origin that involves both genetic and environmental factors. Several studies showed that excess body fat increased the risk of multiple comorbidities, such as high blood pressure, coronary heart disease, type 2 diabetes, insulin resistance, and cancer. According to the results of the research, the mother's nutritional status and obesogenic environments have a great influence on childhood obesity. A summary of the results of many studies concluded that childhood obesity is more likely to develop non-communicable diseases in adulthood. The global prevalence of overweight in children aged 5 years or under has increased modestly, but with heterogeneous trends in low and middle-income regions, while the prevalence of obesity in children aged 2–4 years has increased moderately. Overweight or obesity during childhood has important short-term and long-term consequences. Conclusion In recent decades, the prevalence of obesity in children has increased dramatically. For the successful implementation of activities to prevent overweight and obesity in children, it is necessary to create a supportive environment and to promote health.

Tissue fibrosis, characterized by excessive accumulation of aberrant extracellular matrix (ECM) produced by myofibroblasts, is a growing cause of mortality worldwide. Understanding the factors that induce myofibroblastic differentiation is paramount to prevent or reverse the fibrogenic process. Integrin-mediated interaction between the ECM and cytoskeleton promotes myofibroblast differentiation. In the present study, we explored the significance of integrin alpha 11 (ITGA11), the integrin alpha subunit that selectively binds to type I collagen during tissue fibrosis in the liver, lungs and kidneys. We showed that ITGA11 was co-localized with α-smooth muscle actin-positive myofibroblasts and was correlatively induced with increasing fibrogenesis in mouse models and human fibrotic organs. Furthermore, transcriptome and protein expression analysis revealed that ITGA11 knockdown in hepatic stellate cells (liver-specific myofibroblasts) markedly reduced transforming growth factor β-induced differentiation and fibrotic parameters. Moreover, ITGA11 knockdown dramatically altered the myofibroblast phenotype, as indicated by the loss of protrusions, attenuated adhesion and migration, and impaired contractility of collagen I matrices. Furthermore, we demonstrated that ITGA11 was regulated by the hedgehog signaling pathway, and inhibition of the hedgehog pathway reduced ITGA11 expression and fibrotic parameters in human hepatic stellate cells in vitro, in liver fibrosis mouse model in vivo and in human liver slices ex vivo. Therefore, we speculated that ITGA11 might be involved in fibrogenic signaling and might act downstream of the hedgehog signaling pathway. These findings highlight the significance of the ITGA11 receptor as a highly promising therapeutic target in organ fibrosis.
Animals ; Collagen ; Collagen Type I ; Cytoskeleton ; Extracellular Matrix ; Fibrosis ; Hedgehogs ; Hepatic Stellate Cells ; Humans ; In Vitro Techniques ; Kidney ; Liver ; Liver Cirrhosis ; Lung ; Mice ; Mortality ; Myofibroblasts* ; Phenotype* ; Transcriptome ; Transforming Growth Factors