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RESEARCH PRODUCT

Tejido adiposo epicárdico, adiponectina y leptina: Una fuente potencial de riesgo cardiovascular en Enfermedad renal crónica

María Jesús PuchadesLuis D'marcoPaolo RaggiMarcos M. Lima-martínezCarlos SotoMaria Romero-parraJosé Luis GórrizValmore Bermúdez

subject

LeptinPopulationAdipokineAdipose tissue030209 endocrinology & metabolismReview030204 cardiovascular system & hematologyBioinformaticsleptinCatalysislcsh:ChemistryInorganic Chemistry03 medical and health sciences0302 clinical medicinecardiovascular diseaseDiabetes mellitusmedicineHumansRenal Insufficiency ChronicPhysical and Theoretical Chemistryeducationlcsh:QH301-705.5Molecular BiologySpectroscopyeducation.field_of_studyadiponectinAdiponectinbusiness.industryLeptinOrganic ChemistryGeneral MedicineEpicardial Adipose Tissueepicardial adipose tissuemedicine.diseaseCardiovascular diseaseComputer Science ApplicationsAdipose Tissuelcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesAdiponectinMetabolic syndromebusinessPericardiumKidney disease

description

The importance of cardiometabolic factors in the inception and progression of atherosclerotic cardiovascular disease is increasingly being recognized. Beyond diabetes mellitus and metabolic syndrome, other factors may be responsible in patients with chronic kidney disease (CKD) for the high prevalence of cardiovascular disease, which is estimated to be 5- to 20-fold higher than in the general population. Although undefined uremic toxins are often blamed for part of the increased risk, visceral adipose tissue, and in particular epicardial adipose tissue (EAT), have been the focus of intense research in the past two decades. In fact, several lines of evidence suggest their involvement in atherosclerosis development and its complications. EAT may promote atherosclerosis through paracrine and endocrine pathways exerted via the secretion of adipocytokines such as adiponectin and leptin. In this article we review the current knowledge of the impact of EAT on cardiovascular outcomes in the general population and in patients with CKD. Special reference will be made to adiponectin and leptin as possible mediators of the increased cardiovascular risk linked with EAT.