ReviewPPAR research2016
PPARs and Mitochondrial Metabolism: From NAFLD to HCC.
Review in PPAR research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 86 citations in OpenAlex.
- Article
- Revealing improvement mechanism of yak meat quality by dietary withFood chemistry. Molecular sciences · 2026Article
- Therapeutic potential of cannabidiol supplementation in mitigating lipid precursors of inflammation in hepatic steatosis progression.Journal of cannabis research · 2026Article
- The multifaceted role of oral microbiota-host interactions in oral submucous fibrosis: from pathogenic mechanisms to microecological regulation therapies.Frontiers in microbiology · 2026Review
- PPARγ, a key modulator of metabolic reprogramming, stemness and chemoresistance associated with retrodifferentiation in human hepatocellular carcinomas.Cell death & disease · 2025Article
- Review
- Fibromyalgia diagnosis from a multi-omics approach: a gut feeling.Frontiers in microbiology · 2025Article
- Effects of a Sorghum Beverage withFoods (Basel, Switzerland) · 2024Article
- Cannabidiol alleviates carbon tetrachloride-induced liver fibrosis in mice by regulating NF-κB and PPAR-α pathways.Experimental biology and medicine (Maywood, N.J.) · 2024Article
- Gemfibrozil Improves Microcirculatory Oxygenation of Colon and Liver without Affecting Mitochondrial Function in a Model of Abdominal Sepsis in Rats.International journal of molecular sciences · 2023Article
- Effects of Exercise Training on Mitochondrial Fatty Acid β-Oxidation in the Kidneys of Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- Loss of hepatic FTCD promotes lipid accumulation and hepatocarcinogenesis by upregulating PPARγ and SREBP2.JHEP reports : innovation in hepatology · 2023Article
- Comparative Transcriptomic Analysis of Three Common Liver Cell Lines.International journal of molecular sciences · 2023Article
- Pravastatin Improves Colonic and Hepatic Microcirculatory Oxygenation during Sepsis without Affecting Mitochondrial Function and ROS Production in Rats.International journal of molecular sciences · 2023Article
- Key hepatoprotective roles of mitochondria in liver regeneration.American journal of physiology. Gastrointestinal and liver physiology · 2023Review
- Therapeutically targeting essential metabolites to improve immunometabolism manipulation after liver transplantation for hepatocellular carcinoma.Frontiers in immunology · 2023Review
- Bioinformatics Analysis IdentifiesDisease markers · 2023Article
- Review
- Review
- Placental structure, function, and mitochondrial phenotype relate to fetal size in each fetal sex in mice†.Biology of reproduction · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic related diseases, such as type 2 diabetes, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD), are widespread threats which bring about a significant burden of deaths worldwide, mainly due to cardiovascular events and cancer. The pathogenesis of these diseases is extremely complex, multifactorial, and only partially understood. As the main metabolic organ, the liver is central to maintain whole body energetic homeostasis. At the cellular level, mitochondria are the metabolic hub connecting and integrating all the main biochemical, hormonal, and inflammatory signaling pathways to fulfill the energetic and biosynthetic demand of the cell. In the liver, mitochondria metabolism needs to cope with the energetic regulation of the whole body. The nuclear receptors PPARs orchestrate lipid and glucose metabolism and are involved in a variety of diseases, from metabolic disorders to cancer. In this review, focus is placed on the roles of PPARs in the regulation of liver mitochondrial metabolism in physiology and pathology, from NAFLD to HCC.
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.