Evidence mapPaperPMID 41220919Full record

ArticleEXCLI journal2025

Extracellular vesicles and microRNAs in metabolic dysfunction-associated steatotic liver disease: from steatosis to hepatocellular carcinoma.

Melina Belén Keingeski, Larisse Longo, Anelise da Silva Pinto, Bruno de Souza Basso, Thalia Michele Vier Schmitz, Vitória Brum da Silva Nunes, Juliete Nathali Scholl, Camila Kehl Dias, Fabrício Figueiró, Danieli Rosane Dallemole and 9 more

Abstract read
In one paragraph

Article in EXCLI journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

19 authors.

Melina Belén KeingeskiGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Larisse LongoGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Anelise da Silva PintoGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Bruno de Souza BassoGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Thalia Michele Vier SchmitzExperimental Laboratory of Hepatology and Gastroenterology, Center for Experimental Research, Hospital de Clínicas de Porto Alegre, Porto Alegre, Rio Grande do Sul, Brazil.
Vitória Brum da Silva NunesLaboratory of Cancer Immunobiochemistry, Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Juliete Nathali SchollLaboratory of Cancer Immunobiochemistry, Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Camila Kehl DiasLaboratory of Cancer Immunobiochemistry, Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Fabrício FigueiróLaboratory of Cancer Immunobiochemistry, Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Danieli Rosane DallemoleGraduate Program in Pharmaceutical Sciences, Faculty of Pharmacy, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Adriana Raffin PohlmannGraduate Program in Pharmaceutical Sciences, Faculty of Pharmacy, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Isabel Veloso PereiraLaboratório de Investigação Médica (LIM07) do Hospital das Clínicas, da Faculdade de Medicina da Universidade de São Paulo, SP, Brazil.
Jose Tadeu StefanoLaboratório de Investigação Médica (LIM07) do Hospital das Clínicas, da Faculdade de Medicina da Universidade de São Paulo, SP, Brazil.
José Eduardo VargasLaboratory of Inflammatory and Neoplastic Cells, Department of Cell Biology, Section of Biological Sciences, Universidade Federal do Parana, Curitiba, Brazil.
Patrícia Luciana da Costa LopezGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Claudia P OliveiraLaboratório de Investigação Médica (LIM07) do Hospital das Clínicas, da Faculdade de Medicina da Universidade de São Paulo, SP, Brazil.
Juan Pablo ArabDivision of Gastroenterology, Hepatology, and Nutrition, Department of Internal Medicine, Virginia Commonwealth University School of Medicine, Richmond, VA, 23298, USA.
Mário Reis Álvares-da-SilvaGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Carolina Uribe-CruzGraduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EVs) and microRNAs, involved in intercellular communication, have emerged as potential biomarkers in liver diseases. This study aimed to evaluate EV characteristics and microRNA transport across the full spectrum of metabolic dysfunction-associated steatotic liver disease (MASLD). 168 patients with MASLD and 50 controls were recruited. Biochemical and clinical variables were evaluated. EVs were isolated from serum and characterized by nanoparticle tracking analysis, flow cytometry, and Western blotting. Using MiRWalk 3.0 and the TarPmiR algorithm, candidate EV-associated microRNAs related to MASLD were identified. The expression of miR-4758, miR-188, miR-1226, and miR-122, was evaluated in EVs and serum. EV size and concentration varied significantly across disease stages (p<0.001 and p<0.05, respectively), with early MASLD dominated by exosome, and later stages showing a shift toward microvesicles. In MASLD patients, interestingly, miR-122 was lower in EVs compared to serum (p<0.05). In steatosis, it was higher in serum than EVs (p<0.05), without significant differences in later stages. miR-122 in EVs increased in association with GGT and cholesterol, and decreased with elevated creatinine. Serum miR-122 was also elevated in patients with high cholesterol. In MASLD miR-4758 was higher in EVs than in serum (p<0.05), expressed in steatosis and cirrhosis (p<0.05), suggesting it is a good disease marker, and detected exclusively in serum in HCC (p<0.05). miR-4758-EVs increased with high glucose. MiR-188 and miR-1226 were exclusively expressed in serum (p<0.05), and miR-1226 was elevated in patients with high cholesterol. EV size was reduced in individuals with high triglycerides and albumin, suggesting interaction between EVs, biochemical parameters and disease stage. These findings suggest that microRNA expression and transport in EVs and serum vary across MASLD stages and associate with key biochemical parameters, supporting the clinical value of jointly assessing both compartments as potential biomarkers to distinguish early disease from advanced stages such as HCC. See also the graphical abstract(Fig. 1).

Indexed as

cirrhosisextracellular vesicleshepatocellular carcinomametabolic dysfunction-associated steatohepatitismetabolic dysfunction-associated steatotic liver diseasemicroRNAs

Identifiers

PMID41220919
PMCPMC12598109

What Socratic holds

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Registered trials

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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.