Evidence map›Paper›PMID 41673560›Full record

ArticleClinical proteomics2026

Plasma-targeted proteomic and lipidomic profiling of MASLD, MASH, and hepatitis C virus infection.

Suzumi M Tokuoka, Fumie Hamano, Ayako Kobayashi, Masaya Sugiyama, Hirokazu Takahashi, Masashi Mizokami, Yoshiya Oda

Abstract read
In one paragraph

Article in Clinical proteomics, 2026. 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
–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

1 citing paper in PubMed.

  1. 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

7 authors.

Suzumi M TokuokaDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0051, Japan.
Fumie HamanoDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0051, Japan.
Ayako KobayashiDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0051, Japan.
Masaya SugiyamaDepartment of Viral Pathogenesis and Controls, National Institute of Global Health and Medicine, Japan Institute for Health Security, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Hirokazu TakahashiSaga University Hospital, 5-1-1 Nabeshima, Saga, 849-8501, Japan.
Masashi MizokamiDepartment of Viral Pathogenesis and Controls, National Institute of Global Health and Medicine, Japan Institute for Health Security, 1-7-1 Kohnodai, Ichikawa, Chiba, 272-8516, Japan.
Yoshiya OdaDepartment of Lipidomics, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0051, Japan. yoda@m.u-tokyo.ac.jp.

Funding

AMED 23tm0624002j0001JSPS KAKENHI 21K06853
6 · The paper itself

Abstract

backgroundMetabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are chronic liver diseases characterized by lipid accumulation and persistent inflammation, often progressing to fibrosis or hepatocellular carcinoma (HCC). Hepatitis C virus (HCV) infection shares overlapping pathological features, including chronic inflammation and fibrogenesis. Despite their prevalence, reproducible plasma-level molecular data that capture disease-associated systemic alterations remain limited.

methodsWe conducted targeted proteomic and targeted lipidomic profiling of several hundred plasma samples from Japanese patients diagnosed with MASLD, MASH, or HCV infection. Targeted proteomics quantified 184 plasma proteins using the Olink Proximity Extension Assay, and targeted lipidomics quantified approximately 500 phospholipid and triglyceride species using LC/MS-based selected reaction monitoring. Reproducibility was assessed across three independent cohorts.

resultsSeven proteins (CASP-8, CCL20, CTSD, SCF, MMP-3, TRAIL, and TWEAK) consistently differed between MASLD and MASH across all cohorts, reflecting coordinated changes related to apoptosis, inflammation, and immune signaling. Similar alterations were observed in HCV (Hepatitis C virus), indicating shared immune dysregulation. Lipidomic analysis revealed reproducible remodeling characterized by decreased ether-linked phosphatidylethanolamine (PE), increased ester-linked PE, and elevated saturated sphingomyelin (SM) in MASH. Correlation analyses indicate coordinated relationships between selected protein and lipid alterations, including relationships between CTSD and PE and triglyceride (TG) species containing linoleic acid (18:2).

conclusionsThe results of this research provide value to the field of proteomics as a large-scale, reproducible, and hypothesis-generating plasma dual-omics reference dataset. This study was not designed to establish diagnostic biomarkers, to assess clinical discriminative performance, or to imply causal mechanisms. Instead, by emphasizing reproducibility independent cohorts, we provide a plasma dual-omics reference dataset that captures coordinated immune and lipid metabolic alterations associated with chronic liver disease severity. These data provide a framework and resource for future studies researching risk stratification, therapeutic monitoring, and mechanistic validation in chronic liver disease.

Indexed as

Clinical samplesHCVLipidomicsMASHMASLDMulti-omicsPlasmaProteomics

Identifiers

PMID41673560
PMCPMC13179626

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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 OpenQuestion graph.