Affordable Access

Access to the full text

Epicardial Adipose Tissue, Adiponectin and Leptin: A Potential Source of Cardiovascular Risk in Chronic Kidney Disease

Authors
  • D’Marco, Luis1
  • Puchades, Maria Jesús1
  • Gorriz, Jose Luis1
  • Romero-Parra, Maria1
  • Lima-Martínez, Marcos
  • Soto, Carlos
  • Bermúdez, Valmore
  • Raggi, Paolo2
  • 1 (M.R.-P.)
  • 2 Mazankowski Alberta Heart Institute, School of Medicine, University of Alberta, Edmonton, AB T6G 2B7, Canada
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Feb 01, 2020
Volume
21
Issue
3
Identifiers
DOI: 10.3390/ijms21030978
PMID: 32024124
PMCID: PMC7037723
Source
PubMed Central
Keywords
License
Green

Abstract

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.

Report this publication

Statistics

Seen <100 times