ArticleNature immunology2020
IL-1 induces mitochondrial translocation of IRAK2 to suppress oxidative metabolism in adipocytes.
Article in Nature immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 57 citations in OpenAlex.
- Innate immune signalling in the adipocyte.Journal of biochemistry · 2026Review
- Article
- Genome wide DNA methylation and transcriptome integration analysis reveals potential markers in type A aortic dissection pathogenesis.Scientific reports · 2025Article
- IRAK signaling in cancers: mechanisms, targeting, and clinical implications.Expert opinion on investigational drugs · 2025Review
- DIRAS1 Drives Oxaliplatin Resistance in Colorectal Cancer via PHB1-Mediated Mitochondrial Homeostasis.Biology · 2025Article
- Integrating SNP data to reveal the adaptive selection features of goat populations in extreme environments.BMC genomics · 2025Article
- Review
- Impact of 4-Environment & health (Washington, D.C.) · 2025Article
- IL-1 protects from fatal systemic candidiasis in mice by inhibiting oxidative phosphorylation and hypoxia.Nature communications · 2025Article
- Exploration of non-coding RNAs related to intramuscular fat deposition Xinjiang Brown cattle and Angus × Wagyu cattle.BMC genomics · 2025Article
- RBM43 controls PGC1α translation and a PGC1α-STING signaling axis.Cell metabolism · 2025Article
- Inflammatory Gene Expression in Livers Undergoing Ex Situ Normothermic Perfusion Is Attenuated by Leukocyte Removal From the Perfusate.Transplantation · 2025Article
- Eye on the horizon: The metabolic landscape of the RPE in aging and disease.Progress in retinal and eye research · 2025Review
- IL-1β promotes adipogenesis by directly targeting adipocyte precursors.Nature communications · 2024Article
- Unraveling the complex roles of macrophages in obese adipose tissue: an overview.Frontiers of medicine · 2024Review
- The immunometabolic function of VGLL3 and female-biased autoimmunity.Immunometabolism (Cobham, Surrey) · 2024Review
- LncRNA LINK-A Remodels Tissue Inflammatory Microenvironments to Promote Obesity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Alleviating mitochondrial dysfunction in diabetic cardiomyopathy through the Adipsin and Irak2 pathways.Military Medical Research · 2024Article
- Interleukin-1 receptor associated kinase 2 is a functional downstream regulator of complement factor D that controls mitochondrial fitness in diabetic cardiomyopathy.Military Medical Research · 2024Article
- L-arginine metabolism inhibits arthritis and inflammatory bone loss.Annals of the rheumatic diseases · 2024Article
Corrections and comments
- Commented on by
Authors and funding
22 authors at 5 institutions in 3 countries.
Funding
Abstract
Chronic inflammation is a common feature of obesity, with elevated cytokines such as interleukin-1 (IL-1) in the circulation and tissues. Here, we report an unconventional IL-1R-MyD88-IRAK2-PHB/OPA1 signaling axis that reprograms mitochondrial metabolism in adipocytes to exacerbate obesity. IL-1 induced recruitment of IRAK2 Myddosome to mitochondria outer membranes via recognition by TOM20, followed by TIMM50-guided translocation of IRAK2 into mitochondria inner membranes, to suppress oxidative phosphorylation and fatty acid oxidation, thereby attenuating energy expenditure. Adipocyte-specific MyD88 or IRAK2 deficiency reduced high-fat-diet-induced weight gain, increased energy expenditure and ameliorated insulin resistance, associated with a smaller adipocyte size and increased cristae formation. IRAK2 kinase inactivation also reduced high-fat diet-induced metabolic diseases. Mechanistically, IRAK2 suppressed respiratory super-complex formation via interaction with PHB1 and OPA1 upon stimulation of IL-1. Taken together, our results suggest that the IRAK2 Myddosome functions as a critical link between inflammation and metabolism, representing a novel therapeutic target for patients with obesity.
Indexed as
Identifiers
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.