Another microRNA related to cell differentiation and proliferation is miR145. La Rocca et al. demonstrated that miR-145 expression is increased during cell differentiation. A 2009 study conducted on cell cultures of pre-adipocytes and differentiating adipocytes of obese individuals demonstrated that the expression of miR-145 was greatly reduced during cell differentiation. In the present study, the expression of miR-143 and miR-145 did not differ between obese individuals and non-obese controls. We expected to detect an increased expression of miR-143 and miR-145 in all tissues of the obese group compared to control since these microRNAs are related to increased cell differentiation and proliferation, but this was not the case. On the other hand, there was a negative correlation between the expression of miR-145 and LEPR in the omentum of obese patients. In a critical evaluation of this article, the limited number of patients included in each group, mainly because of the limited grant dedicated to it, must have interfered in the statistical analysis. New study with more patients is now being planned and also with the possibility to include other microRNAs. On the basis of the present data, we may conclude that there was a negative correlation between the expression of miR-145 and LEPR in the omentum of obese patients. This allows us to Saikosaponin-C affirm that miR-145 may play a role in the regulation of obesity. New studies, with larger casuistic, are needed to confirm the real envolvement of the microRNAs with obesity. Alterations in arterial structure and function occur with advancing age in healthy individuals, and the aging-induced decrease in endothelial function contributes to the increases in arterial stiffness. Several studies have shown that arterial stiffness is lower in physically active individuals compared with sedentary individuals. Furthermore, aerobic exercise training reduces arterial stiffness, which increases with advancing age. Thus, regular aerobic exercise prevents or reduces arterial stiffness. Nitric oxide, which is produced from Larginine by endothelial NO synthase in endothelial cells, contributes to the underlying mechanism of this effect of exercise. NO Rosiridin causes vasodilation and inhibits the development of arteriosclerosis and atherosclerosis. Aging impairs arterial eNOS protein and mRNA expression, however, eNOS expression levels are increased by endurance exercise training in aged rats. Moreover, in middle-aged and older woman, moderate regular exercise training elevates plasma NOx levels with reduction of blood pressure. Thus, aging impairs NO 
bioavailability, and it may result in increased arterial stiffness. Recently, apelin has been detected in several tissues, such as white adipose tissue, kidney, heart, and vessel. Apelin is initially synthesized as preproapelin, which consists of 77 aminoacid residues. Following enzymatic cleavage, the C-terminus is released into the circulation as the biologically active fragment, apelin. Apelin acts via APJ receptor in the expressing endothelial cells. Clinical evidence suggests that plasma apelin levels are generally lower in patients with cardiovascular diseases, such as heart failure and hypertension. In animal studies, apelin administration decreased blood pressure in normal and hypertensive rats.