PLoS One
March 2024
Atherosclerotic Cardiovascular Disease (ASCVD) represents the leading cause of death worldwide, and individual screening should be based on behavioral, metabolic, and genetic profile derived from data collected in large population-based studies. Due to the polygenic nature of ASCVD, we aimed to assess the association of genomics with ASCVD risk and its impact on the occurrence of acute myocardial infarction, stroke, or peripheral artery thrombotic-ischemic events at population level. CardioVascular Genes (CV-GENES) is a nationwide, multicenter, 1:1 case-control study of 3,734 patients in Brazil.
View Article and Find Full Text PDFAtherosclerosis is the biological basis of ischemic heart disease and ischemic stroke, the leading causes of death in the world. After decades of studies, the understanding of atherosclerosis has evolved dramatically, and inflammation has been recognized as one of the most relevant pillars in all phases of atherosclerotic disease. Nevertheless, only recently, the trial CANTOS, and subsequent outcome studies with colchicine, finally provided proof-of-concept evidence that anti-inflammatory therapies were able to reduce cardiovascular events with no influence on lipid levels.
View Article and Find Full Text PDFPurpose Of Review: The purpose of this review was to summarize important and updated information on sitosterolemia. Sitosterolemia is an inherited lipid disorder consisting of high levels of plasma plant sterols. This sterol storage condition is caused by biallelic loss-of-function genetic variants in either ABCG5 or ABCG8, leading to increased intestinal absorption and decreased hepatic excretion of plant sterols.
View Article and Find Full Text PDFBackground: Sitosterolemia is a rare autosomal recessive disorder caused by homozygous or compound heterozygous variants in . The disease is characterized by increased plasma plant sterols. Small case series suggest that patients with sitosterolemia have wide phenotypic heterogeneity with great variability on either plasma cholesterol levels or development of atherosclerotic cardiovascular disease.
View Article and Find Full Text PDFAm J Med Genet C Semin Med Genet
December 2020
Diabetol Metab Syndr
September 2017
[This corrects the article DOI: 10.1186/s13098-017-0225-1.].
View Article and Find Full Text PDFAlthough patients with diabetes have 2 to 4 times increased risk of cardiovascular morbidity and mortality than individuals without diabetes, recent studies indicate that a significant part of patients are in a lower cardiovascular risk category. Men younger than 35 years, women younger than 45 years, patients with diabetes duration of less than 10 years without other risk factors have a much lower risk than patients who have traditional cardiovascular risk factors, and subclinical or established coronary artery disease (CAD). These patients are not risk equivalent as stated in previous studies.
View Article and Find Full Text PDFIntroduction: the use of statins is associated with reduced cardiovascular risk in studies of primary and secondary prevention, and the reduction is directly proportional to the reduction of LDL-cholesterol. Recent evidence suggests that statins may be associated with a higher incidence of new cases of diabetes. The aim of this review is to explore this possibility, identifying factors associated with the increase in risk and the potential diabetogenic mechanisms of statins.
View Article and Find Full Text PDFObjective: Obesity associates with increased numbers of inflammatory cells in adipose tissue (AT), including T cells, but the mechanism of T-cell recruitment remains unknown. This study tested the hypothesis that the chemokine (C-X-C motif) receptor 3 (CXCR3) participates in T-cell accumulation in AT of obese mice and thus in the regulation of local inflammation and systemic metabolism.
Approach And Results: Obese wild-type mice exhibited higher mRNA expression of CXCR3 in periepididymal AT-derived stromal vascular cells compared with lean mice.
Obesity, long considered a condition characterized by the deposition of inert fat, is now recognized as a chronic and systemic inflammatory disease, where adipose tissue plays a crucial endocrine role through the production of numerous bioactive molecules, collectively known as adipokines. These molecules regulate carbohydrate and lipid metabolism, immune function and blood coagulability, and may serve as blood markers of cardiometabolic risk. Local inflammatory loops operate in adipose tissue as a consequence of nutrient overload, and crosstalk among its cellular constituents-adipocytes, endothelial and immune cells-results in the elaboration of inflammatory mediators.
View Article and Find Full Text PDFAdipose tissue (AT) can accumulate macrophages and secrete several inflammatory mediators. Despite its pivotal role in the progression of chronic inflammatory processes such as atherosclerosis, the adaptive role of immunity in obesity remains poorly explored. Visceral AT of diet-induced obese C57BL/6 mice had higher numbers of both CD4(+) and CD8(+) T cells than lean controls, monitored by flow cytometry.
View Article and Find Full Text PDFAfter a long history of relative neglect by the scientific community, white adipose tissue is finally emerging as a central component of body homeostasis. Indeed, the explosion of obesity statistics worldwide encouraged the study of adipose tissue and the complications of increased adiposity, such as insulin resistance, type 2 diabetes, and accelerated vascular disease. Far beyond merely furnishing free fatty acids from triglyceride depots, a growing list of fat tissue-derived mediators has increased the understanding of the regulatory role of adipose tissue in metabolic control.
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