Download
1 / 29
0 likes | 54 Views
Types and rule of adipokinase in the pathogenesis of CVD
E N D
Rule of Adipokines in the cardiovascular disease Professor/Mohammed Ahmed Bamashmos
Introduction Cardiovascular disease (CVD) is the greatest cause of death, accounting for nearly one-third of all deaths worldwide. The increase in obesity rates over 3 decades is widespread and threatens the public health in both developed and developing countries. Obesity, the excessive accumulation of visceral fat, causes the clustering of metabolic disorders, such as type 2 diabetes, dyslipidemia, and hypertension, culminating in the development of CVD.
Adipose tissue is not only an energy storage organ, but an active endocrine tissue producing various biologically active proteins known as adipokines. Since leptin, a central regulator of food intake and energy expenditure, was demonstrated to be an adipose-specific adipokine, attention has focused on the identification and characterization of unknown adipokines to clarify the mechanisms underlying obesity-related disorders
Numerous adipokines have been identified in the past 2 decades; most adipokines are upregulated in the obese state. Adipokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and resistin are pro-inflammatory, and exacerbate various metabolic and cardiovascular diseases. However, a small number of adipokines, including adiponectin, are decreased by obesity, and generally exhibit antiinflammatory properties and protective functions against obesity-related diseases. Collectively, an imbalance in the production of pro- and antiinflammatory adipokines in the obese condition results in multiple complications. In this review, we focus on the pathophysiologic roles of adipokines with cardiovascular protective properties.
Ample evidence from both clinical and experimental settings supports the role for obesity in the pathogenesis of CVD, including heart failure (HF) (72, 87, 89, 94–106). Not only is obesity closely intertwined with greater prevalence of coexisting risk factors for CVD such as coronary artery disease, hypertension, diabetes mellitus, and obstructive sleep apnea (2, 3), but obesity alone also impacts myocardial structure and pump performance (manifestations of obesity cardiomyopathy) (107).
More recently, a new term “cardiometabolic-based chronic disease” (CMBCD) was introduced to boost timely and continued preventive care for cardiometabolic diseases rooted from genetics, environment, and behavior cues. Reported endpoints for CMBCD encompass coronary heart disease, heart failure, and atrial fibrillation (AF), all of which are commonly present in obesity (108). Early evidence for obesity-related CVD includes findings from the Framingham Heart Study that demonstrated an elevated risk of coronary disease, stroke,
More recently, a new term “cardiometabolic-based chronic disease” (CMBCD) was introduced to boost timely and continued preventive care for cardiometabolic diseases rooted from genetics, environment, and behavior cues. Reported endpoints for CMBCD encompass coronary heart disease, heart failure, and atrial fibrillation (AF), all of which are commonly present in obesity (108). Early evidence for obesity-related CVD includes findings from the Framingham Heart Study that demonstrated an elevated risk of coronary disease, stroke,
Adipokines and Cardiovascular Risk Adipose tissue is increasingly recognized as an endocrine organ, capable of remotely signaling to other tissues to alter their metabolic program. This signaling is accomplished through the secretion by adipocytes of numerous factors generally referred to as adipokines, and including molecules, such as leptin, adiponectin, chemerin, and others. Adipokines have a wide range of metabolic effects, including the regulation of insulin sensitivity, inflammation, fibrosis, appetite, and blood pressure.21 Given the vast array of metabolic effects of adipokines, there is great interest in the contribution of adipokines to cardiovascular risk and multiple novel mechanisms through which adipokines contribute to coronary heart disease (CHD) have recently been described
