ReviewThe Journal of endocrinology2023
Role of hepatic peroxisome proliferator-activated receptor γ in non-alcoholic fatty liver disease.
Review in The Journal of endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Peroxisome proliferator-activated receptor gamma (PPARγ) as a mechano-metabolic transducer: coordinating lipid homeostasis through mechanical cues.Molecular biomedicine · 2026Review
- Hepatocyte-specific PPARγ Deletion Uncovers Role of an Antagonistic PPARγ-HNF4α Transcriptional Axis in Metabolic Dysfunction-Associated Steatotic Liver Disease Progression.The American journal of pathology · 2026Article
- Hepatoprotection of Jianpi Qingre Lishi prescription on non-alcoholic steatohepatitis miRNA-27/peroxisome proliferator-activated receptor gamma axis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Dynamic modelling of liver-bone axis: A microphysiological approach to hepatic osteodystrophy.Bioactive materials · 2026Article
- PPARγ-dependent and -independent regulation of methionine metabolism by diet-induced obesity and fasting in male mice.bioRxiv : the preprint server for biology · 2026Article
- Comparative study of obeticholic acid and rosuvastatin in high-fat/fructose diet-induced metabolic dysfunction: role of AMPK, PPAR-γ, SREBP-1c, and STAT3 pathways.Journal of molecular histology · 2026Article
- Loss of BATF3 impairs adipose-liver homeostasis and accelerates the transition from steatosis to fibrosis in high-fat diet-fed mice.International journal of biological sciences · 2026Article
- PPARγ-dependent and -independent regulation of genes involved in hepatic methionine cycle in fasted or diet-induced obese mice.PloS one · 2026Article
- GATA-Biology · 2025Article
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- Article
- The role of ubiquitination and deubiquitination in the pathogenesis of non-alcoholic fatty liver disease.Frontiers in immunology · 2025Review
- Research Progress on the Role and Mechanism of Flavonoids in Improving Metabolic Associated Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- ASPP2 deficiency attenuates lipid accumulation through the PPARγ pathway in alcoholic liver injury.Cell biology and toxicology · 2024Article
- LncRNAeLife · 2024Article
- Silibinin Targeting Heat Shock Protein 90 Represents a Novel Approach to Alleviate Nonalcoholic Fatty Liver Disease by Simultaneously Lowering Hepatic Lipotoxicity and Enhancing Gut Barrier Function.ACS pharmacology & translational science · 2024Article
- Chronic Hepatitis C Virus Infection, Extrahepatic Disease and the Impact of New Direct-Acting Antivirals.Pathogens (Basel, Switzerland) · 2024Review
- Multi-ancestry polygenic mechanisms of type 2 diabetes.Nature medicine · 2024Article
- Multi-ancestry Polygenic Mechanisms of Type 2 Diabetes Elucidate Disease Processes and Clinical Heterogeneity.Research square · 2023Article
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
Peroxisome proliferator-activated receptor γ (PPARγ) belongs to a family of nuclear receptors that could serve as lipid sensors. PPARγ is the target of a group of insulin sensitizers called thiazolidinediones (TZDs) which regulate the expression of genes involved in glucose and lipid metabolism as well as adipokines that regulate metabolic function in other tissues. Non-alcoholic fatty liver disease (NAFLD) has a high prevalence worldwide and is even higher in patients with obesity and insulin resistance. TZD-mediated activation of PPARγ could serve as a good treatment for NAFLD because TZDs have shown anti-fibrogenic and anti-inflammatory effectsin vitro and increase insulin sensitivity in peripheral tissues which improves liver pathology. However, mechanistic studies in mouse models suggest that the activation of PPARγ in hepatocytes might reduce or limit the therapeutic potential of TZD against NAFLD. In this review, we briefly describe the short history of PPAR isoforms, the relevance of their expression in different tissues, as well as the pathogenesis and potential therapeutics for NAFLD. We also discuss some evidence derived from mouse models that could be useful for endocrinologists to assess tissue-specific roles of PPARs, complement reverse endocrinology approaches, and understand the direct role that PPARγ has in hepatocytes and non-parenchymal cells.
Indexed as
Identifiers
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.