ArticleNature communications2024
Adipose tissue macrophage infiltration and hepatocyte stress increase GDF-15 throughout development of obesity to MASH.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Large-Scale Plasma Proteomics Enhances Prediction of Liver-Related Events Among Individuals With Prediabetes and Type 2 Diabetes: A Prospective Cohort Study in the UK Biobank.Diabetes, obesity & metabolism · 2026Article
- Plasma GDF-15 Levels Are Associated With HIV Reservoir Markers Independently of Inflammation in People With HIV on Antiretroviral Therapy.The Journal of infectious diseases · 2026Article
- Deep behavioral phenotyping reveals novel features in a mouse model of metabolic dysfunction-associated steatohepatitis.Scientific reports · 2026Article
- GDF15 in Liver Fibrosis: Molecular Mechanisms, Immunoregulatory Functions, and Therapeutic Potential.Biomolecules · 2026Review
- ZFP90 Serves as a Transcriptional Brake on NF-κB Signaling to Attenuate Diet-Induced MASLD Progression.Nutrients · 2026Article
- Endothelial GDF15 deficiency enhances barrier function and mitigates pulmonary fibrosis.JCI insight · 2026Article
- Adipokine-mediated metabolic responses across BMI in acute myocardial infarction.BMC cardiovascular disorders · 2026Article
- Western diet-induced MASH in PWK/PhJ mice identifies disruptions in amino acid and sphingolipid metabolism contributing to cardiac dysfunction.Nature communications · 2026Article
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
- Research progress on the biological function and molecular mechanism of GDF-15 in solid malignant tumors.World journal of surgical oncology · 2026Review
- Hepatocyte estrogen-related receptor α modulates a gluconeogenic-epigenetic crosstalk counteracting MASLD/MASH progression.Experimental & molecular medicine · 2026Article
- Dysregulation of the Gut-Adipose Tissue-Liver Axis: a Possible Mechanism Behind the Relationship Between Metabolic Dysfunction-Associated Steatotic Liver Disease and Type 2 Diabetes.Current diabetes reports · 2026Review
- The impact of bariatric and metabolic surgery on the levels of circulating growth differentiation factor 15 in humans.Journal of physiology and biochemistry · 2026Review
- Growth differentiation factor 15: from stress response to clinical utility in chronic liver diseases.Journal of gastroenterology · 2026Review
- KBN2202 Suppresses Gonadal White Adipose Tissue Expansion in Female Mice Fed a High-Fat Diet.International journal of molecular sciences · 2026Article
- Pleiotropic effects of GDF-15 to regulate nutritional status: perspectives from body composition to nutrition-related disorders.British journal of biomedical science · 2026Review
- GDF15 as a sentinel of metabolic integrity: a narrative review of stress signaling, multisystem pathophysiology, and therapeutic potential.Frontiers in endocrinology · 2026Review
- Growth Differentiation Factor 15 (GDF-15) as a modulator of hepatic steatosis and fibrosis: insights from a 6-year retrospective cohort study.Frontiers in medicine · 2026Article
- The upregulation of GDF15 is controlled epigenetically by oncogenic TCF19 signaling in human hepatocellular carcinoma.iScience · 2025Article
- The Impact of Antidiabetic Therapy on Liver Injury, Steatosis, and Fibrosis in Patients with Type 2 Diabetes and Metabolic Dysfunction-Associated Steatotic Liver Disease.Medicina (Kaunas, Lithuania) · 2025Observational
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20 authors.
Funding
Abstract
Plasma growth differentiation factor-15 (GDF-15) levels increase with obesity and metabolic dysfunction-associated steatotic liver disease (MASLD) but the underlying mechanism remains poorly defined. Using male mouse models of obesity and MASLD, and biopsies from carefully-characterized patients regarding obesity, type 2 diabetes (T2D) and MASLD status, we identify adipose tissue (AT) as the key source of GDF-15 at onset of obesity and T2D, followed by liver during the progression towards metabolic dysfunction-associated steatohepatitis (MASH). Obesity and T2D increase GDF15 expression in AT through the accumulation of macrophages, which are the main immune cells expressing GDF15. Inactivation of Gdf15 in macrophages reduces plasma GDF-15 concentrations and exacerbates obesity in mice. During MASH development, Gdf15 expression additionally increases in hepatocytes through stress-induced TFEB and DDIT3 signaling. Together, these results demonstrate a dual contribution of AT and liver to GDF-15 production in metabolic diseases and identify potential therapeutic targets to raise endogenous GDF-15 levels.
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