ArticleNature communications2016
The transcriptional coregulator GRIP1 controls macrophage polarization and metabolic homeostasis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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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
32 citing papers in PubMed, 48 citations in OpenAlex.
- A transcriptional cofactor GRIP1 drives PPARγ DNA binding and p300-dependent enhancer activity during homeostatic macrophage polarization.Science advances · 2026Article
- Steroid receptor coactivators: from basic research to translational opportunities.Endocrine reviews · 2026Review
- Steroid receptor coactivators in immunity - From function to emerging translational opportunities.The Journal of biological chemistry · 2026Review
- GSDME-IL-18 pyroptotic axis prevents myosteatosis by expanding tissue-resident macrophages to promote muscle regeneration.The Journal of clinical investigation · 2026Article
- HNF4A mitigates sepsis-associated lung injury by upregulating NCOR2/GR/STAB1 axis and promoting macrophage polarization towards M2 phenotype.Cell death & disease · 2025Article
- The FcRn from gene to protein and function: comparison between species.Frontiers in immunology · 2025Review
- Disrupting the RNA polymerase II transcription cycle through CDK7 inhibition ameliorates inflammatory arthritis.Science translational medicine · 2024Article
- Mechanisms of epigenomic and functional convergence between glucocorticoid- and IL4-driven macrophage programming.Nature communications · 2024Article
- Mechanisms of Epigenomic and Functional Convergence Between Glucocorticoid- and IL4-Driven Macrophage Programming.bioRxiv : the preprint server for biology · 2024Article
- Macrophage polarization: an important role in inflammatory diseases.Frontiers in immunology · 2024Review
- Xinyang tablet ameliorates sepsis-induced myocardial dysfunction by regulating Beclin-1 to mediate macrophage autophagy and M2 polarization through LncSICRNT1 targeting E3 ubiquitin ligase TRAF6.Chinese medicine · 2023Article
- Modulating glucocorticoid receptor actions in physiology and pathology: Insights from coregulators.Pharmacology & therapeutics · 2023Review
- A human model of asthma exacerbation reveals transcriptional programs and cell circuits specific to allergic asthma.Science immunology · 2023Article
- Adipose tissue macrophages as potential targets for obesity and metabolic diseases.Frontiers in immunology · 2023Review
- Early diagnosis for the onset of peri-implantitis based on artificial neural network.Open life sciences · 2023Article
- The chromosome-scale genome of the raccoon dog: Insights into its evolutionary characteristics.iScience · 2022Article
- Steroid receptor coactivators - their role in immunity.Frontiers in immunology · 2022Review
- Physiological Convergence and Antagonism Between GR and PPARγ in Inflammation and Metabolism.Advances in experimental medicine and biology · 2022Review
- Areca catechu-(Betel-nut)-induced whole transcriptome changes in a human monocyte cell line that may have relevance to diabetes and obesity; a pilot study.BMC endocrine disorders · 2021Article
- Chemical systems biology reveals mechanisms of glucocorticoid receptor signaling.Nature chemical biology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Diet-induced obesity causes chronic macrophage-driven inflammation in white adipose tissue (WAT) leading to insulin resistance. WAT macrophages, however, differ in their origin, gene expression and activities: unlike infiltrating monocyte-derived inflammatory macrophages, WAT-resident macrophages counteract inflammation and insulin resistance, yet, the mechanisms underlying their transcriptional programming remain poorly understood. We recently reported that a nuclear receptor cofactor-glucocorticoid receptor (GR)-interacting protein (GRIP)1-cooperates with GR to repress inflammatory genes. Here, we show that GRIP1 facilitates macrophage programming in response to IL4 via a GR-independent pathway by serving as a coactivator for Kruppel-like factor (KLF)4-a driver of tissue-resident macrophage differentiation. Moreover, obese mice conditionally lacking GRIP1 in macrophages develop massive macrophage infiltration and inflammation in metabolic tissues, fatty livers, hyperglycaemia and insulin resistance recapitulating metabolic disease. Thus, GRIP1 is a critical regulator of immunometabolism, which engages distinct transcriptional mechanisms to coordinate the balance between macrophage populations and ultimately promote metabolic homeostasis.
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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.