A special type of stem cells, defined as endothelial progenitor cells (EPCs), has been found in the bone marrow and peripheral blood. These EPCs are incorporated into injured vessels and become mature endothelial cells during re-endothelialization and neovascularization processes. Though a complete phenotypic description of EPCs remains unclear, these cells express several surface markers, the most relevant including CD34 and CD133 antigens. Furthermore, EPCs derived from other sources could also give rise to mature endothelial cells, which makes this group of cells more diverse. The recruitment of EPCs from the bone marrow to homing sites of vasculogenesis is subject to regulation by many factors, including chemokines and growth factors. The precise mechanism of EPC mobilization and differentiation is not entirely elucidated and is still under investigation. Recent studies have suggested that EPCs may promote local angiogenesis by secreting angiogenic growth factors in a paracrine manner. The number and function of EPCs can be affected during pathological conditions, including diabetes mellitus, cardiovascular risk factors for ischemic disease, and graft vasculopathy. Additionally, EPC number and migration capacity could be improved by such factors as drugs, physical exercise, and growth factors. Transplantation of EPCs into ischemic tissues may emerge as a promising approach in the therapy of diseases associated with blood vessel disorders.
The prevalence of obesity continues to grow rapidly worldwide, posing many public health challenges of the 21st century. Obese subjects are at major risk for serious diet-related noncommunicable diseases, including type 2 diabetes mellitus, cardiovascular disease, and non-alcoholic fatty liver disease. Understanding the mechanisms underlying obesity pathogenesis is needed for the development of effective treatment strategies. Dysregulation of incretin secretion and actions has been observed in obesity and related metabolic disorders; therefore, incretin-based therapies have been developed to provide new therapeutic options. Incretin mimetics present glucose-lowering properties, together with a reduction of appetite and food intake, resulting in weight loss. In this review, we describe the physiology of two known incretins—glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), and their role in obesity and related cardiometabolic disorders. We also focus on the available and incoming incretin-based medications that can be used in the treatment of the above-mentioned conditions.
Our results suggest that Hcy might increase carotid artery IMT by reducing EPCs numbers. Possible involvement of Hcy in the reduction of EPCs number in hypertensive patients might be in part mediated by Hcy influence on the TAS.
Background:The pleiotropic effects of hypotensive drugs should always be taken into consideration. There is limited data on the effect of such drugs on reducing global cardiovascular risk in young hypertensives. The aim of this study was to evaluate the effect of nebivolol and ramipril on biochemical parameters, arterial stiffness, and circadian profile of blood pressure (BP) in young men undergoing treatment for hypertension (HT).Methods:A total of 80 patients aged 16 to 28 years of age with grade 1 HT were enrolled into the prospective randomized, open-label trial. They were randomized to receive 5 mg of nebivolol or 5 mg of ramipril, daily. Arterial stiffness index (SI), the circadian profile of BP registered in ambulatory blood pressure monitoring (ABPM), and biochemical parameters—including lipid profile, insulinemia, glycemia, and high sensitivity C-reactive protein (hsCRP) levels—were evaluated before and after the twelve-week period.Results:After the treatment period, we observed significant decreases in both ABPM systolic blood pressure (SBP) in group of nebivolol (P = .0007) and ramipril (P = .0001) and in ABPM diastolic blood pressure (DBP) in group of nebivolol (P = .0018) and ramipril (P = .0006). Reductions in the nondippers percentage were found in group of nebivolol and ramipril (P = .0077, P = .0001 respectively). Ramipril treatment resulted in a significant plausible modification in high-density lipoprotein (HDL) (P = .0390), glucose (P = .0213), and hsCRP (P = .0053) concentrations, as well as decreased SI (P = .0009) value, while nebivolol treatment showed no such benefits.Conclusions:Despite the similar hypotensive effect of nebivolol and ramipril, ramipril seems to possess better clinical potential in reducing cardiovascular risk in young men with HT.
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