Evidence mapPaperPMID 37895151Full record

ReviewInternational journal of molecular sciences2023

Metabolic-Dysfunction-Associated Steatotic Liver Disease-Its Pathophysiology, Association with Atherosclerosis and Cardiovascular Disease, and Treatments.

Hidekatsu Yanai, Hiroki Adachi, Mariko Hakoshima, Sakura Iida, Hisayuki Katsuyama

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 4 pooled it
24.2field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 4 syntheses or guidelines pooled it, 114 citations in OpenAlex.

  1. Guideline
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  5. Trial
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  7. Autophagy in MASLD: A Metabolic and Precision Medicine Perspective.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Review
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44 more citing papers are in PubMed but not listed here.

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

5 authors at 1 institution in 1 country.

Hidekatsu YanaiDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Japan.ORCID 0000-0002-4199-3665
Hiroki AdachiDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Japan.
Mariko HakoshimaDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Japan.
Sakura IidaDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Japan.
Hisayuki KatsuyamaDepartment of Diabetes, Endocrinology and Metabolism, National Center for Global Health and Medicine, Kohnodai Hospital, 1-7-1 Kohnodai, Ichikawa 272-8516, Japan.ORCID 0000-0003-2871-8340
National Center for Global Health and Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metabolic-dysfunction-associated steatotic liver disease (MASLD) is a chronic liver disease that affects more than a quarter of the global population and whose prevalence is increasing worldwide due to the pandemic of obesity. Obesity, impaired glucose metabolism, high blood pressure and atherogenic dyslipidemia are risk factors for MASLD. Therefore, insulin resistance may be closely associated with the development and progression of MASLD. Hepatic entry of increased fatty acids released from adipose tissue, increase in fatty acid synthesis and reduced fatty acid oxidation in the liver and hepatic overproduction of triglyceride-rich lipoproteins may induce the development of MASLD. Since insulin resistance also induces atherosclerosis, the leading cause for death in MASLD patients is cardiovascular disease. Considering that the development of cardiovascular diseases determines the prognosis of MASLD patients, the therapeutic interventions for MASLD should reduce body weight and improve coronary risk factors, in addition to an improving in liver function. Lifestyle modifications, such as improved diet and increased exercise, and surgical interventions, such as bariatric surgery and intragastric balloons, have shown to improve MASLD by reducing body weight. Sodium glucose cotransporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 receptor agonists (GLP-1RAs) have been shown to improve coronary risk factors and to suppress the occurrence of cardiovascular diseases. Both SGLT2i and GLP-1 have been reported to improve liver enzymes, hepatic steatosis and fibrosis. We recently reported that the selective peroxisome proliferator-activated receptor-alpha (PPARα) modulator pemafibrate improved liver function. PPARα agonists have multiple anti-atherogenic properties. Here, we consider the pathophysiology of MASLD and the mechanisms of action of such drugs and whether such drugs and the combination therapy of such drugs could be the treatments for MASLD.

Indexed as

AtherosclerosisCardiovascular DiseasesFatty LiverInsulin ResistanceSodium-Glucose Transporter 2 InhibitorsFatty AcidsHumansObesityPPAR alphaFatty AcidsPPAR alphaSodium-Glucose Transporter 2 Inhibitorscardiovascular diseasefatty acidsinsulin resistancemetabolic-dysfunction-associated steatotic liver diseasepemafibratetriglyceride

Identifiers

PMID37895151
PMCPMC10607514
OpenAlexW4387878772

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.