Evidence map›Paper›PMID 40474196›Full record

ReviewCell & bioscience2025

Post-translational modifications in the pathophysiological process of metabolic dysfunction‑associated steatotic liver disease.

Yiyang Min, Yiqiao Zhang, Yu Ji, Shanshan Liu, Chengjian Guan, Luyang Wei, Huajing Yu, Zhongtao Zhang

Abstract readReview
In one paragraph

Review in Cell & bioscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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.

Yiyang Min *Department of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China.
Yiqiao Zhang *Department of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China.
Yu Ji *Department of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China.
Shanshan LiuDepartment of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China.
Chengjian GuanDepartment of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China.
Luyang WeiDepartment of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China. lywei@mail.ccmu.edu.cn.
Huajing YuDepartment of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China. huajingyu@pku.edu.cn.
Zhongtao ZhangDepartment of General Surgery, Beijing Friendship Hospital, State Key Lab of Digestive Health & National Clinical Research Center for Digestive Diseases, Capital Medical University, Beijing, 100050, China. zhangzht@ccmu.edu.cn.

Funding

Beijing Postdoctoral Research Foundation 2022-ZZ-004Capital's Funds for Health Improvement and Research 2020-1-2021Capital's Funds for Health Improvement and Research 2024-1-1192China Postdoctoral Science Foundation 2023M732411National Key Technologies Research and Development Program 2015BAI13B09National Natural Science Foundation of China 82070580National Natural Science Foundation of China 82200964
6 · The paper itself

Abstract

In recent years, the prevalence of metabolic dysfunction‑associated steatotic liver disease (MASLD), which was called non-alcoholic fatty liver disease (NAFLD), has been progressively increasing in populations. The progression of MASLD encompasses a spectrum from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), and ultimately to cirrhosis or even hepatocellular carcinoma. During the early stages of the disease, lipid accumulation and endoplasmic reticulum stress may lead to abnormalities in hepatic DNA expression, protein synthesis, and post-translational modifications (PTMs). PTMs play a crucial role in the progression of MASLD and include histone and non-histone modifications, with major types including methylation, acetylation, ubiquitination, and phosphorylation. Numerous studies indicate that within MASLD-related signaling pathways, PTMs can modulate protein activity, localization, folding, and interactions by altering their physicochemical properties. This review summarizes various significant PTMs involved in MASLD progression to elucidate the regulatory mechanisms and pathogenesis associated with the disease.

Indexed as

Histone proteinMetabolic dysfunction‑associated steatotic liver disease (MASLD)Non-histone proteinPost-translational modifications (PTMs)

Identifiers

PMID40474196
PMCPMC12143077

What OpenQuestion holds

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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 OpenQuestion graph.