ReviewAnimals : an open access journal from MDPI2020
Identification of Crucial Genetic Factors, Such as PPARγ, that Regulate the Pathogenesis of Fatty Liver Disease in Dairy Cows Is Imperative for the Sustainable Development of Dairy Industry.
Review in Animals : an open access journal from MDPI, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- Identification of fecal microbes as potential biomarkers for early diagnosis of fatty liver disease in cattle.Virulence · 2025Article
- Choline attenuates NEFA-induced hepatic steatosis via GNMT regulation in hepatocytes.Stress biology · 2025Article
- Forage Carbohydrate Profiles and Endocrine Morphometric Interactions in Traditionally Managed Horses from Romania.Life (Basel, Switzerland) · 2025Article
- Ameliorative Effect of Heat-KilledJournal of microbiology and biotechnology · 2025Article
- Down-regulation of miR-29 improves lipid metabolism in fatty liver of dairy cows.Animal biotechnology · 2024Article
- Application of PPAR Ligands and Nanoparticle Technology in Metabolic Steatohepatitis Treatment.Biomedicines · 2024Review
- Menin orchestrates hepatic glucose and fatty acid uptake via deploying the cellular translocation of SIRT1 and PPARγ.Cell & bioscience · 2023Article
- Comprehensive review of resveratrol as a feed additive in dairy cows: exploring its potential diverse effects and implications.Veterinary research communications · 2023Review
- Comparison of protective effects of hesperetin and pectolinarigenin on high-fat diet-induced hyperlipidemia and hepatic steatosis in Golden Syrian hamsters.Experimental animals · 2023Article
- Article
- The Occurrence of a Negative Energy Balance in Holstein-Friesian and Simmental Cows and Its Association with the Time of Resumption of Reproductive Activity.Metabolites · 2022Article
- Obesity-Related Metabolic Dysfunction in Dairy Cows and Horses: Comparison to Human Metabolic Syndrome.Life (Basel, Switzerland) · 2021Review
- Proteome analysis identified proteins associated with mitochondrial function and inflammation activation crucially regulating the pathogenesis of fatty liver disease.BMC genomics · 2021Article
- Protein acetylation in mitochondria plays critical functions in the pathogenesis of fatty liver disease.BMC genomics · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Frequently occurring fatty liver disease in dairy cows during the perinatal period, a typical type of non-alcoholic fatty liver disease (NAFLD), results in worldwide high culling rates of dairy cows (averagely about 25%) after calving. This has been developing into a critical industrial problem throughout the world, because the metabolic disease severely affects the welfare and economic value of dairy cows. Findings about the molecular mechanisms how the fatty liver disease develops would help scientists to discover novel therapeutic targets for NAFLD. Studies have shown that PPARγ participates or regulates the fat deposition in liver by affecting the biological processes of hepatic lipid metabolism, insulin resistance, gluconeogenesis, oxidative stress, endoplasmic reticulum stress and inflammation, which all contribute to fatty liver. This review mainly focuses on crucial regulatory mechanisms of PPARγ regulating lipid deposition in the liver via direct and/or indirect pathways, suggesting that PPARγ might be a potential critical therapeutic target for fatty liver disease, however, it would be of our significant interest to reveal the pathology and pathogenesis of NAFLD by using dairy cows with fatty liver as an animal model. This review will provide a molecular mechanism basis for understanding the pathogenesis of NAFLD.
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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.