ArticleCell metabolism2019
Aging Induces an Nlrp3 Inflammasome-Dependent Expansion of Adipose B Cells That Impairs Metabolic Homeostasis.
Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05975528 (Effect of Sodium-glucose Cotransporter-2 Inhibitor in Cellular Senescence in Patients With Cardiovascular Diseases or Advanced Type 2 Diabetes), which is not on this map. Cited by 146 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.
Effect of Sodium-glucose Cotransporter-2 Inhibitor in Cellular Senescence in Patients With Cardiovascular Diseases or Advanced Type 2 Diabetes
Who cites it
146 citing papers in PubMed, 207 citations in OpenAlex.
- Age-Associated B Cells: Origins, Regulation, and Tissue-Specific Pathogenic Contributions in Autoimmune, Metabolic, and Neurological Diseases.Immunological reviews · 2026Review
- The ageing immune system as a driver of systemic ageing.Nature reviews. Immunology · 2026Review
- Nuclear-Mitochondria Crosstalk in Senescent Adipose-Derived Stem Cells.Smart medicine · 2026Review
- Mechanism and therapeutic prospects of adipose tissue B lymphocytes in obesity and obesity‑associated metabolic diseases (Review).Molecular medicine reports · 2026Review
- Pck1 Deficiency Drives Mitochondrial Dysfunction and Cellular Senescence in Adipocytes.Aging cell · 2026Article
- The value of targeting ketone body metabolism in inflammatory and autoimmune diseases.Journal of translational medicine · 2026Review
- Immunometabolic resistors of aging in long-lived golden spiny mice.Science advances · 2026Article
- Adipocytes as core drivers of skin aging and novel targets for regeneration.Biogerontology · 2026Review
- Interleukin-10 expressing B lineage cells in visceral adipose tissue protect against aging-related insulin resistance and extend lifespan.Nature communications · 2026Article
- Immune Aging as a Failure of Programmed Cell Death Coordination.International journal of molecular sciences · 2026Review
- B cells drive CD4 T cell immunosenescence and age-associated health decline.Science immunology · 2026Article
- Age-associated B-cells across the rheumatoid arthritis continuum: from early immunopathogenesis to comorbidities.Frontiers in aging · 2026Review
- The life cycle of tertiary lymphoid structures in pancreatic cancer-a window of opportunity for immunotherapy.Frontiers in immunology · 2026Review
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- GDF3 promotes adipose tissue macrophage-mediated inflammation via altered chromatin accessibility during aging.Nature aging · 2026Article
- Immunoglobulin G in aging and cancer.Frontiers in immunology · 2026Review
- Article
- Adipose immune microenvironment: catalyst of age-related adipose tissue dysfunction.Immunity & ageing : I & A · 2025Review
- Immunometabolic Crosstalk in Adipose Tissue Remodeling: Mechanisms and Therapeutic Perspectives.Journal of obesity & metabolic syndrome · 2025Review
- Adipocytes are dispensable in shaping the ovarian cancer tumor microenvironment in the omentum.bioRxiv : the preprint server for biology · 2025Article
86 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
During aging, visceral adiposity is often associated with alterations in adipose tissue (AT) leukocytes, inflammation, and metabolic dysfunction. However, the contribution of AT B cells in immunometabolism during aging is unexplored. Here, we show that aging is associated with an expansion of a unique population of resident non-senescent aged adipose B cells (AABs) found in fat-associated lymphoid clusters (FALCs). AABs are transcriptionally distinct from splenic age-associated B cells (ABCs) and show greater expansion in female mice. Functionally, whole-body B cell depletion restores proper lipolysis and core body temperature maintenance during cold stress. Mechanistically, the age-induced FALC formation, AAB, and splenic ABC expansion is dependent on the Nlrp3 inflammasome. Furthermore, AABs express IL-1R, and inhibition of IL-1 signaling reduces their proliferation and increases lipolysis in aging. These data reveal that inhibiting Nlrp3-dependent B cell accumulation can be targeted to reverse metabolic impairment in aging AT.
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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.