The guides in this section are maintained by Brett H.īrett is the Founder of and he's been helping people improve their computer skills since the 1990's. Operating Systems - Latest version numbers: The latest version of Internet Explorer.What are the latest versions of Browsers & Plugins? Web Browsers - Latest version numbers: What happens if you don't update your browser?.Why it's good to keep your browser up to dateĪre we telling you to update, but you have the latest version?Īre there any risks with updating Chrome? Wondering why you even need to bother updating?

What does it actually mean to update your browser?ĭo you need to do anything, or is it automatic? HDACs: histone deacetylases HDAC4: histone deacetylase 4 DNMT1: DNA methyltransferase 1 Pitx2c: paired-like homeodomain transcription factor 2, isoform c.Frequently asked questions about updating your web browser These molecular mechanisms lead to atrial fibrillation and heart failure. HDAC4 is a master negative regulator of cardiac hypertrophy, where it is found oxidized, triggering de-repression of pro-hypertrophy genes like myocyte enhancement factor 2 (MEF2) and serum response factor (SRF). Specifically, increased methylation in Pitx2c and sarco/endoplasmic reticulum Ca 2+ ATPase (SERCA) promoters provoke a decrease in expression, contributing to heart failure pathophysiology. These events up-regulate DNMT1 and, in consequence, lead to DNA hypermethylation. Visceral obesity causes systemic chronic inflammation and deregulation in hypoxia inducible factor 3 (HIF3), fat mass and obesity-associated protein (FTO), and brain derived neurotrophic factor (BDNF) gene methylation, as well as serum TNF-α increase. PPARs animal models biomarkers cardiovascular diseases epigenetic modifications gut microbiota dysbiosis obesity pathophysiology therapeutic treatments.ĭNA and histone modifications in obesity-linked cardiac dysfunction. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975.

Up to date