Evidence map›Paper›PMID 32024124›Full record

ReviewInternational journal of molecular sciences2020

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

Luis D'Marco, Maria Jesús Puchades, Jose Luis Gorriz, Maria Romero-Parra, Marcos Lima-Martínez, Carlos Soto, Valmore Bermúdez, Paolo Raggi

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Journal of diabetes research · 2020
    Pooled it
  2. Abnormal "Frontiers in cardiovascular medicine · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 4 countries.

Luis D'MarcoNephrology Department, Hospital Clínico Universitario, INCLIVA, University of Valencia, 46010 Valencia, Spain.ORCID 0000-0003-0148-891X
Maria Jesús PuchadesNephrology Department, Hospital Clínico Universitario, INCLIVA, University of Valencia, 46010 Valencia, Spain.
Jose Luis GorrizNephrology Department, Hospital Clínico Universitario, INCLIVA, University of Valencia, 46010 Valencia, Spain.
Maria Romero-ParraNephrology Department, Hospital Clínico Universitario, INCLIVA, University of Valencia, 46010 Valencia, Spain.
Marcos Lima-MartínezPhysiologic Sciences Department, School of Health Sciences, Universidad de Oriente, Bolívar 5110, Venezuela.
Carlos SotoNephrology Department, Consorci Sanitari del Alt Penedes-Garraf, 08800 Barcelona, Spain.
Valmore BermúdezFacultad de Ciencias de la Salud, Universidad Simón Bolívar, Barranquilla 080005, Colombia.ORCID 0000-0003-1880-8887
Paolo RaggiMazankowski Alberta Heart Institute, School of Medicine, University of Alberta, Edmonton, AB T6G 2B7, Canada.ORCID 0000-0002-5766-1948
Universitat de València · ESConsorci Sanitari Garraf · ESUniversidad de Oriente · VEUniversidad Simón Bolívar · COUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AdiponectinAdipose TissueCardiovascular DiseasesHumansLeptinPericardiumRenal Insufficiency, ChronicAdiponectinADIPOQ protein, humanLeptinAdiponectincardiovascular diseaseepicardial adipose tissueleptin

Identifiers

PMID32024124
PMCPMC7037723
OpenAlexW3003676396

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.