ArticlePPAR research2013
Peroxisome proliferator-activated receptor genetic polymorphisms and nonalcoholic Fatty liver disease: any role in disease susceptibility?
Article in PPAR research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses 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
15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 27 citations in OpenAlex.
- Pooled it
- Meta-analysis of associations between the peroxisome proliferator-activated receptor-γ Pro12Ala polymorphism and susceptibility to nonalcoholic fatty liver disease, rheumatoid arthritis, and psoriatic arthritis.Genetic testing and molecular biomarkers · 2014Pooled it
- Aerobic exercise improved liver steatosis by modulating miR-34a-mediated PPARα/SIRT1-AMPK signaling pathway.PloS one · 2025Article
- Partitioned polygenic risk scores identify distinct types of metabolic dysfunction-associated steatotic liver disease.Nature medicine · 2024Article
- Article
- Impact of PPAR-Alpha Polymorphisms-The Case of Metabolic Disorders and Atherosclerosis.International journal of molecular sciences · 2019Review
- The Pro12Ala polymorphism in the PPAR-γ2 gene is not associated with an increased risk of NAFLD in Iranian patients with type 2 diabetes mellitus.Cellular & molecular biology letters · 2019Article
- The genetic backgrounds in nonalcoholic fatty liver disease.Clinical journal of gastroenterology · 2018Review
- Increased parenchymal damage and steatohepatitis in Caucasian non-alcoholic fatty liver disease patients with common IL1B and IL6 polymorphisms.Alimentary pharmacology & therapeutics · 2016Article
- PNPLA3 Expression Is Related to Liver Steatosis in Morbidly Obese Women with Non-Alcoholic Fatty Liver Disease.International journal of molecular sciences · 2016Article
- Effect of miR-34a in regulating steatosis by targeting PPARα expression in nonalcoholic fatty liver disease.Scientific reports · 2015Article
- Genetic Factors in the Pathogenesis of Nonalcoholic Fatty Liver and Steatohepatitis.BioMed research international · 2015Review
- Nonalcoholic fatty liver disease: a comprehensive review of a growing epidemic.World journal of gastroenterology · 2014Review
- Nonalcoholic fatty liver disease: molecular pathways and therapeutic strategies.Lipids in health and disease · 2013Review
- Article
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
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fatty liver disease (NAFLD) defines a wide spectrum of liver diseases that extend from simple steatosis, that is, increased hepatic lipid content, to nonalcoholic steatohepatitis (NASH), a condition that may progress to cirrhosis with its associated complications. Nuclear hormone receptors act as intracellular lipid sensors that coordinate genetic networks regulating lipid metabolism and energy utilization. This family of transcription factors, in particular peroxisome proliferator-activated receptors (PPARs), represents attractive drug targets for the management of NAFLD and NASH, as well as related conditions such as type 2 diabetes and the metabolic syndrome. The impact on the regulation of lipid metabolism observed for PPARs has led to the hypothesis that genetic variants within the human PPARs genes may be associated with human disease such as NAFLD, the metabolic syndrome, and/or coronary heart disease. Here we review the available evidence on the association between PPARs genetic polymorphism and the susceptibility to NAFLD and NASH, and we provide a meta-analysis of the available evidence. The impact of PPAR variants on the susceptibility to NASH in specific subgroup of patients, and in particular on the response to therapies, especially those targeting PPARs, represents promising new areas of investigation.
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.