ArticleNature communications2018
Reduced oxidative capacity in macrophages results in systemic insulin resistance.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 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
108 citing papers in PubMed, 166 citations in OpenAlex.
- GDF-15 levels in patients with polycystic ovary syndrome treated with metformin: a combined clinical and in silico pathway analysis.Archives of endocrinology and metabolism · 2024Trial
- Serine protease inhibitor from Trichinella spiralis ameliorates diet-induced obesity and adipose tissue inflammation through TIM-3-dependent macrophage reprogramming.PLoS pathogens · 2026Article
- 5-methoxytryptamine improves hepatic inflammation and insulin resistance in a macrophage C-X-C motif chemokine ligand 14 dependent manner.Molecular biomedicine · 2026Article
- Baseline Plasma Growth-differentiation Factor 15 and Recovery of Physical Function Following Total Knee Replacement in the Study of Physical Resilience and Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Article
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Growth Differentiation Factor-15 as a Biomarker of Diabetic Complications in Patients with Type 2 Diabetes.Journal of clinical medicine · 2026Article
- The Role of GDF-15 in Heart Failure and Biomarker Potential-From Basic Science to Clinical Praxis.Biology · 2026Review
- Circulating GDF15 and HbA1c Response to Add-On Exenatide Therapy in Type 2 Diabetes: A Post Hoc Analysis from a Multicenter Trial.Biomedicines · 2026Article
- Growth differentiation factor 15 - a new molecular target in inflammatory bowel disease: Progress and challenges.World journal of gastroenterology · 2026Article
- HDAC3-driven immunometabolic reprogramming in type 2 diabetes and its complications: from enzymatic deacetylation to non-enzymatic scaffolding.Frontiers in immunology · 2026Review
- 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
- Thyroid follicular cell-derived GDF15 attenuates inflammation and lipid dysregulation in Hashimoto's thyroiditis.Frontiers in medicine · 2026Article
- Article
- Induction of TFEB promotes Kupffer cell survival and reduces lipid accumulation in MASLD.Hepatology communications · 2025Article
- Revisiting the role of GDF15 in atherosclerosis in mouse and human.Acta pharmacologica Sinica · 2025Article
- BNIP3-mediated mitophagy in macrophages regulates obesity-induced adipose tissue metaflammation.Autophagy · 2025Article
- Red ginseng extract enhances mitochondrial function and alleviates immunosenescence in T cells.Journal of ginseng research · 2025Article
- The association between serum growth differentiation factor 15 and insulin resistance in women diagnosed with polycystic ovary syndrome.Scientific reports · 2025Article
- Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 7 institutions in 3 countries.
Funding
Abstract
Oxidative functions of adipose tissue macrophages control the polarization of M1-like and M2-like phenotypes, but whether reduced macrophage oxidative function causes systemic insulin resistance in vivo is not clear. Here, we show that mice with reduced mitochondrial oxidative phosphorylation (OxPhos) due to myeloid-specific deletion of CR6-interacting factor 1 (Crif1), an essential mitoribosomal factor involved in biogenesis of OxPhos subunits, have M1-like polarization of macrophages and systemic insulin resistance with adipose inflammation. Macrophage GDF15 expression is reduced in mice with impaired oxidative function, but induced upon stimulation with rosiglitazone and IL-4. GDF15 upregulates the oxidative function of macrophages, leading to M2-like polarization, and reverses insulin resistance in ob/ob mice and HFD-fed mice with myeloid-specific deletion of Crif1. Thus, reduced macrophage oxidative function controls systemic insulin resistance and adipose inflammation, which can be reversed with GDF15 and leads to improved oxidative function of macrophages.
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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.