ArticleJournal of hepatology2017
PARP1-mediated PPARα poly(ADP-ribosyl)ation suppresses fatty acid oxidation in non-alcoholic fatty liver disease.
Article in Journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 92 citations in OpenAlex.
- Few-shot learning-driven discovery of Lutein suppresses Th1-mediated inflammation via glucose metabolism.Acta pharmacologica Sinica · 2026Article
- Article
- SOCS3 Stabilizes PARP1 to Suppress Adipogenic Transcription and Abdominal Adipogenesis in Avian.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Hepatic Sirt2-PARP1-HMGB1 axis promotes exercise-mediated amelioration of MASH in mice.Science China. Life sciences · 2026Article
- The Pathophysiological Interrelationship Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2026Review
- PARP inhibitors target cellular energy metabolism: Mechanisms of action and clinical implications.Translational oncology · 2026Review
- Regulated necrosis at the crossroads of liver inflammation and cancer development.Nature reviews. Gastroenterology & hepatology · 2026Review
- SRY mediates male-specific susceptibility to acute liver injury.Cell communication and signaling : CCS · 2025Article
- PARP‑1 in liver diseases: Molecular mechanisms, therapeutic potential and emerging clinical applications (Review).Molecular medicine reports · 2025Review
- NAD + in fatty liver disease: mechanistic insights and associated targets.Cell biology and toxicology · 2025Review
- Role of Macrophage PARP1 in the Regulation of Crosstalk between Adipose Immune Cells and Adipocytes during Diet-induced Obesity.bioRxiv : the preprint server for biology · 2025Article
- ExermiR-129-3p Enhances Muscle Function by Improving Mitochondrial Activity Through PARP1 Inhibition.Journal of cachexia, sarcopenia and muscle · 2025Article
- Multiomics Analysis of Liver Molecular Dysregulation Leading to Nonviral-Related Hepatocellular Carcinoma Development.Journal of proteome research · 2025Article
- The General Principle of the Warburg Effect as a Possible Approach for Cancer Immunotherapy: The Regulatory Effect of Plant Extracts Could Change the Game.Molecules (Basel, Switzerland) · 2025Review
- Metabolic reprogramming of CAR T cells: a new frontier in cancer immunotherapy.Frontiers in immunology · 2025Review
- Temporal regulation of acetylation status determines PARP1 role in DNA damage response and metabolic homeostasis.Science advances · 2024Article
- Intermittent Fasting Regulates Metabolic Homeostasis and Improves Cardiovascular Health.Cell biochemistry and biophysics · 2024Review
- Respiratory Virus-Induced PARP1 Alters DC Metabolism and Antiviral Immunity Inducing Pulmonary Immunopathology.Viruses · 2024Article
- Poly(ADP-ribose) polymerase (PARP)-targeted PET imaging in non-oncology application: a pilot study in preclinical models of nonalcoholic steatohepatitis.American journal of nuclear medicine and molecular imaging · 2024Article
- Disrupting Poly(ADP-ribosyl)ating Pathway Creates Premalignant Conditions in Mammalian Liver.International journal of molecular sciences · 2023Article
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsPARP1 is a key mediator of cellular stress responses and critical in multiple physiological and pathophysiological processes of cells. However, whether it is involved in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) remains elusive.
methodsWe analysed PARP1 activity in the liver of mice on a high fat diet (HFD), and samples from NAFLD patients. Gain- or loss-of-function approaches were used to investigate the roles and mechanisms of hepatic PARP1 in the pathogenesis of NAFLD.
resultsPARP1 is activated in fatty liver of HFD-fed mice. Pharmacological or genetic manipulations of PARP1 are sufficient to alter the HFD-induced hepatic steatosis and inflammation. Mechanistically we identified peroxisome proliferator-activated receptor α (PPARα) as a substrate of PARP1-mediated poly(ADP-ribosyl)ation. This poly(ADP-ribosyl)ation of PPARα inhibits its recruitment to target gene promoters and its interaction with SIRT1, a key regulator of PPARα signaling, resulting in suppression of fatty acid oxidation upregulation induced by fatty acids. Moreover, we show that PARP1 is a transcriptional repressor of PPARα gene in human hepatocytes, and its activation suppresses the ligand (fenofibrate)-induced PPARα transactivation and target gene expression. Importantly we demonstrate that liver biopsies of NAFLD patients display robust increases in PARP activity and PPARα poly(ADP-ribosyl)ation levels.
conclusionsOur data indicate that PARP1 is activated in fatty liver, which prevents maximal activation of fatty acid oxidation by suppressing PPARα signaling. Pharmacological inhibition of PARP1 may alleviate PPARα suppression and therefore have therapeutic potential for NAFLD. LAY SUMMARY: PARP1 is activated in the non-alcoholic fatty liver of mice and patients. Inhibition of PARP1 activation alleviates lipid accumulation and inflammation in fatty liver of mice.
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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.