ArticleCell reports2025
The adiponectin-PPARγ axis in hepatic stellate cells regulates liver fibrosis.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed.
- Metabolic drivers of MASLD and MASH: from hormonal imbalance to fibrosis.Diabetologia · 2026Review
- Hepatic neurons and metabolically induced liver dysfunction.Nature reviews. Endocrinology · 2026Review
- Role of adipocytes and their derived extracellular vesicles in the progression, diagnosis and treatment of liver diseases (Review).International journal of molecular medicine · 2026Review
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Pachymic acid exhibits synergistic antitumor efficacy with lenvatinib in hepatocellular carcinoma by targeting PPARγ to inhibit glycolysis.Medical oncology (Northwood, London, England) · 2026Article
- Physical activity delays ovarian aging in part through adiponectin-related signaling pathways.Nature aging · 2026Article
- Interorgan Crosstalk in MASLD: A Narrative Review.Biomedicines · 2026Review
- Non-enzymatic hepatic ABHD6 interacts with Akt-FoxO1 axis to regulate metabolic health.Nature communications · 2026Article
- Fasting insulin to HDL-C ratio is correlated with MASLD severity in Chinese overweight/obesity: a cross-sectional analysis.BMC endocrine disorders · 2026Article
- Review
- GSTM3 Knockdown Promotes Liver Fibrosis Reversal by Inhibiting Hepatic Stellate Cell Activation via PPARγ Signaling.Journal of clinical and translational hepatology · 2026Article
- Peroxisomes in Liver Diseases: From Metabolite Quality Control to Inter-Organelle and Inter-Organ Signaling.Biomolecules · 2026Review
- Kinase signaling in liver disease via clinical-trial-on-a-PamChip: A distinctive methodology for drug mechanisms and personalized medicine.The Journal of biological chemistry · 2026Article
- Brown adipose tissue inactivation exacerbates alcohol-induced liver steatosis, inflammation, and fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Adiponectin Inhibits Oxidative Stress and Tight Junction Protein Loss: Evidence from a Hepatic Encephalopathy Mouse Model and Brain Endothelial Cells.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Visceral adiposity, metabolic health and aging.Nature aging · 2026Review
- Non-enzymatic ABHD6 interacts with Akt-FoxO1 axis to regulate selective hepatic insulin resistance.bioRxiv : the preprint server for biology · 2026Article
- Microbiome-derived cancer: the catabolism of bilirubin to urobilin in the liver-gut axis and its consequences.Gastroenterology report · 2026Review
- The context-dependent roles of PPAR-γ in adipocyte differentiation and obesity: a master regulator with dual functions.Frontiers in nutrition · 2026Review
- Bilirubin Hepatic and Intestinal Transport and Catabolism: Physiology, Pathophysiology, and Benefits.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Hepatic stellate cells (HSCs) are key drivers of local fibrosis. Adiponectin, conventionally thought of as an adipokine, is also expressed in quiescent HSCs. However, the impact of its local expression on the progression of liver fibrosis remains unclear. We recently generated a transgenic mouse line (Lrat-rtTA) that expresses the doxycycline-responsive transcriptional activator rtTA under the control of the HSC-specific lecithin retinol acyltransferase (Lrat) promoter, which enables us to specifically and inducibly overexpress or eliminate genes in these cells. The inducible elimination of HSCs protects mice from methionine/choline-deficient (MCD) diet-induced liver fibrosis, confirming their causal involvement in fibrosis development. We generated HSC-specific adiponectin overexpression and null models that demonstrate that HSC-specific adiponectin overexpression dramatically reduces liver fibrosis, whereas HSC-specific adiponectin elimination accelerates fibrosis progression. We identify a local adiponectin-peroxisome proliferator-activated receptor gamma (PPARγ) axis in HSCs that exerts a marked influence on the progression of local fibrosis, independent of circulating adiponectin derived from adipocytes.
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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.