ArticleAging cell2020
Aging-induced aberrant RAGE/PPARα axis promotes hepatic steatosis via dysfunctional mitochondrial β oxidation.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Hepatocyte Growth Hormone Receptor Ablation Is Associated With Aging Phenotypes and Hepatic Mitochondrial Dysfunction.Aging cell · 2026Article
- Mesenchymal Stem Cell-Derived Exosomes Improve Aging-Related Changes in Liver Lipid Metabolism by Enhancing Autophagy.Aging cell · 2026Article
- Cholesterol Overload Drives Hepatic Steatosis by Inhibiting OGT-dependent PPARα O-GlcNAcylation and Transactivation.International journal of biological sciences · 2026Article
- Lipid Metabolism-Signaling Crosstalk in Metabolic Disease and Aging: Mechanisms and Therapeutic Targets.Nutrients · 2025Review
- Role of ChREBP-PPARα-FGF21 Axis in Metabolic Dysfunction of MASLD.International journal of molecular sciences · 2025Article
- Aging and metabolic dysfunction-associated steatotic liver disease: a bidirectional relationship.Frontiers of medicine · 2025Review
- Delivering miR-23b-3p by small extracellular vesicles to promote cell senescence and aberrant lipid metabolism.BMC biology · 2025Article
- Age-Dependent Effects of Butyl Benzyl Phthalate Exposure on Lipid Metabolism and Hepatic Fibrosis in Mice.Cells · 2025Article
- CD47-mediated regulation of glucose and lipid metabolism: implications for the pathogenesis of MASLD.Frontiers in endocrinology · 2025Review
- Advanced liver fibrosis, but not MASLD, is associated with accelerated biological aging: a population-based study.BMC public health · 2024Article
- Extracellular vesicles: opening up a new perspective for the diagnosis and treatment of mitochondrial dysfunction.Journal of nanobiotechnology · 2024Review
- Elevated PINK1/Parkin-Dependent Mitophagy and Boosted Mitochondrial Function Mediate Protection of HepG2 Cells from Excess Palmitic Acid by Hesperetin.Journal of agricultural and food chemistry · 2024Article
- Long-term effects of a fat-directed FGF21 gene therapy in aged female mice.Gene therapy · 2024Article
- Trehalose-induced SIRT1/AMPK activation regulates SREBP-1c/PPAR-α to alleviate lipid accumulation in aged liver.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- A biomarker framework for liver aging: the Aging Biomarker Consortium consensus statement.Life medicine · 2024Article
- Inflammaging and fatty acid oxidation in monocytes and macrophages.Immunometabolism (Cobham, Surrey) · 2024Review
- The Roles of Lipid Metabolism in the Pathogenesis of Chronic Diseases in the Elderly.Nutrients · 2023Review
- The Role of Oxidative Stress and Cellular Senescence in the Pathogenesis of Metabolic Associated Fatty Liver Disease and Related Hepatocellular Carcinoma.Antioxidants (Basel, Switzerland) · 2023Review
- Early-onset caloric restriction alleviates ageing-associated steatohepatitis in male mice via restoring mitochondrial homeostasis.Biogerontology · 2023Article
- Biomarkers of aging.Science China. Life sciences · 2023Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD), characterized by an increase in hepatic triglyceride (TG) content, is the most common liver disease worldwide. Aging has been shown to increase susceptibility to NAFLD; however, the underlying molecular mechanism remains poorly understood. In the present study, we examined hepatic TG content and gene expression profiles in body weight-matched young (3 months old), middle-aged (10 months old), and old (20 months old) C57BL/6 mice and found that TGs were markedly accumulated while mitochondrial β-oxidation-related genes, including PPARα, were downregulated in the liver of old mice. In addition, advanced glycation end product receptor (RAGE), a key regulator of glucose metabolism, was upregulated in the old mice. Mechanistically, suppression of RAGE upregulated PPARα and its downstream target genes, which in turn led to reduced TG retention. Finally, we found that hepatic RAGE expression was increased in aging patients, a finding that correlated with decreased PPARα levels. Taken together, our findings demonstrate that the upregulation of RAGE may play a critical role in aging-associated liver steatosis.
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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.