ArticleThe EMBO journal2016
p38γ and p38δ reprogram liver metabolism by modulating neutrophil infiltration.
Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 79 citations in OpenAlex.
- p38γ and p38δ MAP kinases in inflammation.Biochemical Society transactions · 2026Review
- Neutrophil extracellular traps in liver diseases: from molecular mechanisms to therapeutic interventions.Acta pharmacologica Sinica · 2026Review
- Hepatic p38γ exacerbates acetaminophen‑induced acute liver injury via PI3K/Akt‑dependent mechanisms.International journal of molecular medicine · 2026Article
- RNAi-mediated p38δ silencing mitigates anthracycline cardiotoxicity in female mice.American journal of physiology. Heart and circulatory physiology · 2026Article
- Sleep regulates hepatic neutrophil trafficking by modulating uric acid metabolism via sympathetic nervous system activity.bioRxiv : the preprint server for biology · 2026Article
- miR-128-3p and miR-223-3p as Potential Biomarkers of Metabolic Dysfunction in Liver Tissue from Patients Undergoing Metabolic Bariatric Surgery.Obesity surgery · 2026Article
- The Proteome of Exosomes at Birth Predicts Insulin Resistance, Adrenarche and Liver Fat in Childhood.International journal of molecular sciences · 2025Article
- The Evolving Role of Neutrophils and Neutrophil Extracellular Traps (NETs) in Obesity and Related Diseases: Recent Insights and Advances.International journal of molecular sciences · 2024Review
- Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024Review
- Remodeling p38 signaling in muscle controls locomotor activity via IL-15.Science advances · 2024Article
- Lack of p38 activation in T cells increases IL-35 and protects against obesity by promoting thermogenesis.EMBO reports · 2024Article
- From NAFLD to NASH: Understanding the spectrum of non-alcoholic liver diseases and their consequences.Heliyon · 2024Review
- Article
- Neutrophils in Physiology and Pathology.Annual review of pathology · 2024Review
- Role of Mitogen-Activated Protein (MAP) Kinase Pathways in Metabolic Diseases.Genome integrity · 2024Review
- Gossypetin targets the liver-brain axis to alleviate pre-existing liver fibrosis and hippocampal neuroinflammation in mice.Frontiers in pharmacology · 2024Article
- Metabolic Dysfunction-Associated Steatohepatitis Detected by Neutrophilic Crown-Like Structures in Morbidly Obese Patients: A Multicenter and Clinicopathological Study.Research (Washington, D.C.) · 2024Article
- Pirfenidone ameliorates liver steatosis by targeting the STAT3-SCD1 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Review
- Review
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
Abstract
Non-alcoholic fatty liver disease (NAFLD) is a major health problem and the main cause of liver disease in Western countries. Although NAFLD is strongly associated with obesity and insulin resistance, its pathogenesis remains poorly understood. The disease begins with an excessive accumulation of triglycerides in the liver, which stimulates an inflammatory response. Alternative p38 mitogen-activated kinases (p38γ and p38δ) have been shown to contribute to inflammation in different diseases. Here we demonstrate that p38δ is elevated in livers of obese patients with NAFLD and that mice lacking p38γ/δ in myeloid cells are resistant to diet-induced fatty liver, hepatic triglyceride accumulation and glucose intolerance. This protective effect is due to defective migration of p38γ/δ-deficient neutrophils to the damaged liver. We further show that neutrophil infiltration in wild-type mice contributes to steatosis development by means of inflammation and liver metabolic changes. Therefore, p38γ and p38δ in myeloid cells provide a potential target for NAFLD therapy.
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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.