Evidence map›Paper›PMID 41280670›Full record

ReviewiScience2025

Molecular mechanisms mediated by liquid-liquid phase separation in chronic liver disease progression.

Xinran Qiu, Haoyuan Tian, Yuanyuan Gao, Junrui Wang, Zhengyang Bao, Ningyu Qiu, Feng Zhang, Zili Zhang, Feixia Wang, Shizhong Zheng and 1 more

Abstract readReview
In one paragraph

Review in iScience, 2025. 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. 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

11 authors.

Xinran QiuJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Haoyuan TianJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Yuanyuan GaoJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Junrui WangJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Zhengyang BaoJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Ningyu QiuJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Feng ZhangJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Zili ZhangJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Feixia WangJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Shizhong ZhengJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.
Jiangjuan ShaoJiangsu Key Laboratory for Pharmacology and Safety Research of Chinese Materia Media, Nanjing University of Chinese Medicine, Nanjing 210023, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liquid-liquid phase separation (LLPS) is a cellular process driven by multivalent interactions, forming dynamic biomolecular condensates containing proteins, RNAs, and other molecules. LLPS plays a pivotal role in processes such as signal transduction, gene expression, autophagy, and cellular stress responses. The dysregulation of LLPS is linked to chronic liver diseases (CLDs), particularly non-alcoholic fatty liver disease (NAFLD), liver fibrosis, and hepatocellular carcinoma (HCC). LLPS profoundly mediates the pathological evolution of these diseases by regulating key mechanisms, including lipid metabolism, inflammatory responses, and cell death. This review highlights the central role of LLPS in NAFLD progression, liver fibrosis, and HCC transformation. Furthermore, it evaluates the feasibility of targeting LLPS as a therapeutic strategy, proposing innovative approaches such as small-molecule inhibitors, protein modification regulators, and RNA interference to restore LLPS homeostasis. These strategies hold the potential to mitigate disease progression and prevent the transition to fibrosis and liver cancer.

Indexed as

Biological sciencesCell biologyMolecular biology

Identifiers

PMID41280670
PMCPMC12637247

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.