ReviewCells2021
Metabolic Reprogramming of Liver Fibrosis.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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
45 citing papers in PubMed, 73 citations in OpenAlex.
- Gut microbiota metabolic reprogramming drives the development of metabolic diseases in the host.Gut microbes · 2026Review
- Sphingolipid homeostasis and dysregulation in liver function and disease.Life metabolism · 2026Review
- The post-transcriptional regulatory RNA-binding protein PTBP1 functions as an inhibitor in hepatic stellate cell activation and liver fibrosis.Molecular medicine (Cambridge, Mass.) · 2026Article
- Review
- α-Hederin Alleviates Endoplasmic Reticulum Stress by Upregulating TRIM38 Expression, Thereby Inhibiting Hepatic Stellate Cell Activation and Liver Fibrosis.Biomedicines · 2026Article
- Longitudinal characterization of Gaac.1826dupA mice reveals the cardiac, myopathic and biochemical phenotypes of Pompe disease.Disease models & mechanisms · 2026Article
- Comparative urinary metabolomics reveals unique and shared pathways in COVID-19 and liver diseases.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- Elucidating the therapeutic mechanisms of quercetin in hepatic fibrosis: an integrated metabolomic and transcriptomic analysis.Frontiers in nutrition · 2026Article
- Metabolic dysfunction‑associated steatotic liver disease: Pathogenesis, model and treatment (Review).International journal of molecular medicine · 2025Review
- Nanoparticle-based systems for liver therapy: Overcoming fibrosis and enhancing drug efficacy.World journal of hepatology · 2025Review
- Intercellular communication interference through energy metabolism-related exosome secretion inhibition for liver fibrosis treatment.Acta pharmaceutica Sinica. B · 2025Article
- HBV sequence integrated to enhancer acting as oncogenic driver epigenetically promotes hepatocellular carcinoma development.Journal of experimental & clinical cancer research : CR · 2025Article
- Platelet C3G protects from liver fibrosis, while enhancing tumor growth through regulation of the immune response.The Journal of pathology · 2025Article
- Lipid Dysmetabolism in Canine Chronic Liver Disease: Relationship Between Clinical, Histological and Immunohistochemical Features.Veterinary sciences · 2025Article
- RNA binding proteins (RBPs) on genetic stability and diseases.Global medical genetics · 2025Review
- Focal adhesion kinase promotes aerobic glycolysis in hepatic stellate cells via the cyclin D1/c-Myc/MCT-1 pathway to induce liver fibrosis.Scientific reports · 2025Article
- Role of HNF6 in liver homeostasis and pathophysiology.Molecular medicine (Cambridge, Mass.) · 2025Review
- ECM remodeling in hypothyroidism-associated MAFLD: mechanisms, clinical relevance, and therapeutic targets.Frontiers in immunology · 2025Review
- Integrative Multiomics Analysis Identifies HK2 as a Key Regulator of Metabolic Reprogramming in Hepatic Stellate Cells.Human mutation · 2025Article
- The role of non-coding RNA in ferroptosis of liver cancer and its impact on lipid peroxidation.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Liver fibrosis is an excessive and imbalanced deposition of fibrous extracellular matrix (ECM) that is associated with the hepatic wound-healing response. It is also the common mechanism that contributes to the impairment of the liver function that is observed in many chronic liver diseases (CLD). Despite the efforts, no effective therapy against fibrosis exists yet. Worryingly, due to the growing obesity pandemic, fibrosis incidence is on the rise. Here, we aim to summarize the main components and mechanisms involved in the progression of liver fibrosis, with special focus on the metabolic regulation of key effectors of fibrogenesis, hepatic stellate cells (HSCs), and their role in the disease progression. Hepatic cells that undergo metabolic reprogramming require a tightly controlled, fine-tuned cellular response, allowing them to meet their energetic demands without affecting cellular integrity. Here, we aim to discuss the role of ribonucleic acid (RNA)-binding proteins (RBPs), whose dynamic nature being context- and stimuli-dependent make them very suitable for the fibrotic situation. Thus, we will not only summarize the up-to-date literature on the metabolic regulation of HSCs in liver fibrosis, but also on the RBP-dependent post-transcriptional regulation of this metabolic switch that results in such important consequences for the progression of fibrosis and CLD.
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What OpenQuestion 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 OpenQuestion graph.