ReviewiScience2025
Molecular mechanisms mediated by liquid-liquid phase separation in chronic liver disease progression.
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.
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.
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.
Who cites it
1 citing paper in PubMed.
- DHA Targets RAB1B to Mediate the Driving Force Transmission of Copper Ion Vesicular Endocytosis Under Copper Overload for Promoting Cuproptosis and Ferroptosis in Hepatic Stellate Cells.International journal of biological sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
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
Identifiers
What Socratic holds
Registered trials
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.