Evidence map›Paper›PMID 38540305›Full record

ReviewBiomedicines2024

Bridging Metabolic-Associated Steatotic Liver Disease and Cardiovascular Risk: A Potential Role for Ketogenesis.

Rafael Suárez Del Villar-Carrero, Agustín Blanco, Lidia Daimiel Ruiz, Maria J García-Blanco, Ramón Costa Segovia, Rocío García de la Garza, Diego Martínez-Urbistondo

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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

7 authors at 3 institutions in 1 country.

Rafael Suárez Del Villar-CarreroGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.ORCID 0000-0001-8445-6555
Agustín BlancoGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.ORCID 0000-0001-7249-778X
Lidia Daimiel RuizGrupo de Estudio de Nutrigenómica y Nutrición Personalizada, IMDEA Alimentación, 28049 Madrid, Spain.ORCID 0000-0001-9898-6629
Maria J García-BlancoGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.
Ramón Costa SegoviaGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.
Rocío García de la GarzaGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.ORCID 0000-0002-0853-5822
Diego Martínez-UrbistondoGrupo de Riesgo Vascular, Sociedad Española de Medicina Interna (SEMI), 28016 Madrid, Spain.
Sociedad Española de Medicina Interna · ESMadrid Institute for Advanced Studies · ESUniversidad de Alcalá · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The prevalence of cardiovascular diseases (CVDs) is a growing global health concern. Recent advances have demonstrated significant reductions in acute cardiovascular events through the management of modifiable cardiovascular risk factors. However, these factors are responsible for about 50% of the global cardiovascular disease burden. Considering that CVDs are one of the top mortality causes worldwide, the concept of residual cardiovascular risk is an important emerging area of study. Different factors have been proposed as sources of residual risk markers, including non-HDL particles characterization, as well as inflammation measured by serum and imaging technics. Among these, metabolic-associated steatotic liver disease (MASLD) remains controversial. Two opposing viewpoints contend: one positing that fatty liver disease merely reflects classical risk factors and thus adds no additional risk and another asserting that fatty liver disease independently impacts cardiovascular disease incidence. To address this dilemma, one hypothetical approach is to identify specific hepatic energy-yielding mechanisms and assess their impact on the cardiovascular system. Ketogenesis, a metabolic intermediate process particularly linked to energy homeostasis during fasting, might help to link these concepts. Ketogenic metabolism has been shown to vary through MASLD progression. Additionally, newer evidence supports the significance of circulating ketone bodies in cardiovascular risk prediction. Furthermore, ketogenic metabolism modification seems to have a therapeutic impact on cardiovascular and endothelial damage. Describing the relationship, if any, between steatotic liver disease and cardiovascular disease development through ketogenesis impairment might help to clarify MASLD's role in cardiovascular risk. Furthermore, this evidence might help to solve the controversy surrounding liver steatosis impact in CVD and might lead to a more accurate risk assessment and therapeutic targets in the pursuit of precision medicine.

Indexed as

cardiovascular diseasecardiovascular riskketogenesisketone bodiesMASLD

Identifiers

PMID38540305
PMCPMC10968430
OpenAlexW4393003007

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.