ArticleNature2017
Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 287 papers, 2 of them syntheses that pooled it.
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Who cites it
287 citing papers in PubMed, 2 syntheses or guidelines pooled it, 447 citations in OpenAlex.
- Shared and niche-specific transcriptional signatures of macrophage aging revealed by a cross-tissue meta-analysis.BMC biology · 2026Pooled it
- Towards a consensus atlas of human and mouse adipose tissue at single-cell resolution.Nature metabolism · 2025Guideline
- The immunology behind inflammaging-causes, sources, and mechanisms.The Journal of allergy and clinical immunology · 2026Review
- Glycyrrhetinic acid augments lipid catabolism via immune-neural modulation in adipose tissue.Journal of advanced research · 2026Article
- Macrophage-derived itaconate is a negative regulator of adipose tissue thermogenesis.Nature metabolism · 2026Article
- Neurovascular interactions in the ageing heart.Nature reviews. Cardiology · 2026Review
- Nutritional Status-Based Model for Predicting Low-Lactate Shock: A Retrospective Cohort Study.Shock (Augusta, Ga.) · 2026Article
- Stress and the Immune System: Insights From Psychoneuroimmunology.Physiological research · 2026Review
- Regulatory T cells establish an IL-10-IL10Rα immunometabolic checkpoint that limits HSL activation and lipolysis.bioRxiv : the preprint server for biology · 2026Article
- The ageing immune system as a driver of systemic ageing.Nature reviews. Immunology · 2026Review
- Siah2 regulates lipid uptake in adipose tissue macrophages.The Journal of biological chemistry · 2026Article
- The autonomic nervous system in the regulation of glucose and lipid metabolism.Nature reviews. Endocrinology · 2026Review
- Exoproteome of calorie-restricted humans identifies complement deactivation as an immunometabolic checkpoint reducing inflammaging.Nature aging · 2026Article
- Myeloid monoamine oxidase A protects against glucose intolerance, insulin resistance and weight gain in high-fat diet-fed mice by preventing the hyperactivation of macrophages.The Journal of nutritional biochemistry · 2026Article
- ß-adrenergic-like signalling engages CrebB in Drosophila gut to promote female longevity.Nature communications · 2026Article
- Aging disrupts sympathetic innervation of the thymus.Cell reports · 2026Article
- Remnant cholesterol/high-density lipoprotein cholesterol ratio is a new powerful tool for identifying diabetic kidney disease.Journal of diabetes investigation · 2026Article
- Aged Male Mice Remain Glucose Tolerant Despite Increased Energy Storage Efficiency Favoring Diet-Induced Obesity.Aging cell · 2026Article
- S-nitrosoglutathione reductase GSNOR drives age-related obesity by promoting adipose tissue whitening through de-nitrosation of Beclin-1.Nature communications · 2026Article
- Tissue-resident macrophage survival depends on mitochondrial function regulated by SerpinB2 in chronic inflammation.Nature communications · 2026Article
227 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Catecholamine-induced lipolysis, the first step in the generation of energy substrates by the hydrolysis of triglycerides, declines with age. The defect in the mobilization of free fatty acids in the elderly is accompanied by increased visceral adiposity, lower exercise capacity, failure to maintain core body temperature during cold stress, and reduced ability to survive starvation. Although catecholamine signalling in adipocytes is normal in the elderly, how lipolysis is impaired in ageing remains unknown. Here we show that adipose tissue macrophages regulate the age-related reduction in adipocyte lipolysis in mice by lowering the bioavailability of noradrenaline. Unexpectedly, unbiased whole-transcriptome analyses of adipose macrophages revealed that ageing upregulates genes that control catecholamine degradation in an NLRP3 inflammasome-dependent manner. Deletion of NLRP3 in ageing restored catecholamine-induced lipolysis by downregulating growth differentiation factor-3 (GDF3) and monoamine oxidase A (MAOA) that is known to degrade noradrenaline. Consistent with this, deletion of GDF3 in inflammasome-activated macrophages improved lipolysis by decreasing levels of MAOA and caspase-1. Furthermore, inhibition of MAOA reversed the age-related reduction in noradrenaline concentration in adipose tissue, and restored lipolysis with increased levels of the key lipolytic enzymes adipose triglyceride lipase (ATGL) and hormone sensitive lipase (HSL). Our study reveals that targeting neuro-immunometabolic signalling between the sympathetic nervous system and macrophages may offer new approaches to mitigate chronic inflammation-induced metabolic impairment and functional decline.
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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.