ReviewNature reviews. Gastroenterology & hepatology2021
Molecular and cellular mechanisms of liver fibrosis and its regression.
Review in Nature reviews. Gastroenterology & hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,080 papers, 1 of them a synthesis that pooled 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.
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
1,080 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,806 citations in OpenAlex.
- Influenza A Virus (H1N1) Infection Induces Ferroptosis to Promote Developmental Injury in Fetal Tissues.Cell proliferation · 2026Pooled it
- Antifibrotic hydrogel strategies for scarless tissue regeneration: mechanisms, design, and application.Bioactive materials · 2027Review
- Oral self-assembly nanoemulsion drivesDrug delivery · 2026Article
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Breaking the cycle of fibrosis: Ferroptosis as a therapeutic target (Review).International journal of molecular medicine · 2026Review
- Endometriosis and Adenomyosis: Mechanotransduction, Microenvironment, and Mechanisms Beyond Lesions.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Network Pharmacology-Based Prediction and In Vivo Validation of Fumonisin B1-Induced Liver Injury and Early Fibrosis.Journal of biochemical and molecular toxicology · 2026Article
- A human single-cell atlas identifies OLR1Nature genetics · 2026Article
- Vildagliptin attenuates the development of CCl₄-induced liver fibrosis: associations with gut-liver axis modulation and LPS/notch-related signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Engineered Nanoplatforms Targeting Activated Hepatic Stellate Cells for Liver Fibrosis Therapy via TGF-β Axis Inhibition and Ferroptosis Induction.Advanced healthcare materials · 2026Article
- Ginsenosides alleviate the progression of hepatic fibrosis by targeting the liver circadian clock geneMolecular medicine reports · 2026Article
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Role of extracellular matrix in liver fibrosis regression and regeneration (Review).International journal of molecular medicine · 2026Review
- Single-cell RNA Sequencing Analysis Reveals That Targeting PLG-PLGRKT Signaling-mediated Pro-fibrotic Scar-associated Macrophages Ameliorates Liver Fibrosis in Biliary Atresia.Journal of clinical and translational hepatology · 2026Article
- A Hepatocyte-to-Stellate Cell Axis Couples Alternate-Day Fasting to Liver Fibrosis Resolution via ATG7 S-Nitrosylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- [The role of hepatocyte programmed cell death in liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Leveraging serum CHI3L1 and machine learning for non-invasive liver fibrosis diagnostics.iScience · 2026Article
- Reverse bioengineering of the liver: developmental principles for next-generation liver-on-a-chip systems.Communications biology · 2026Review
1,020 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic liver injury leads to liver inflammation and fibrosis, through which activated myofibroblasts in the liver secrete extracellular matrix proteins that generate the fibrous scar. The primary source of these myofibroblasts are the resident hepatic stellate cells. Clinical and experimental liver fibrosis regresses when the causative agent is removed, which is associated with the elimination of these activated myofibroblasts and resorption of the fibrous scar. Understanding the mechanisms of liver fibrosis regression could identify new therapeutic targets to treat liver fibrosis. This Review summarizes studies of the molecular mechanisms underlying the reversibility of liver fibrosis, including apoptosis and the inactivation of hepatic stellate cells, the crosstalk between the liver and the systems that orchestrate the recruitment of bone marrow-derived macrophages (and other inflammatory cells) driving fibrosis resolution, and the interactions between various cell types that lead to the intracellular signalling that induces fibrosis or its regression. We also discuss strategies to target hepatic myofibroblasts (for example, via apoptosis or inactivation) and the myeloid cells that degrade the matrix (for example, via their recruitment to fibrotic liver) to facilitate fibrosis resolution and liver regeneration.
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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.